FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2155347521> ?p ?o ?g. }

• W2155347521 endingPage "694" @default.
• W2155347521 startingPage "691" @default.
• W2155347521 abstract "HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 34, No. 4Recent Highlights of ATVB Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBRecent Highlights of ATVBAneurysms Alan Daugherty and Janet T. Powell Alan DaughertyAlan Daugherty From the Saha Cardiovascular Research Center, University of Kentucky, Lexington (A.D.); and Department of Surgery and Cancer, Imperial College, London, United Kingdom (J.T.P.). Search for more papers by this author and Janet T. PowellJanet T. Powell From the Saha Cardiovascular Research Center, University of Kentucky, Lexington (A.D.); and Department of Surgery and Cancer, Imperial College, London, United Kingdom (J.T.P.). Search for more papers by this author Originally published1 Apr 2014https://doi.org/10.1161/ATVBAHA.114.303353Arteriosclerosis, Thrombosis, and Vascular Biology. 2014;34:691–694IntroductionAortic diseases are common in many populations and are receiving increasing research focus. There are a broad spectrum of aortic diseases that occur in specific regions and appear to have different causes. For example, abdominal aortic aneurysms (AAAs) are most common in aged men.1 In contrast, many forms of thoracic aortic aneurysms (TAAs) occur early in life with a strong genetic basis and no sex discrimination.2 Both aortic aneurysms are amenable to surgical repair. Although surgical approaches have become increasingly sophisticated and less invasive,3 there remains an urgent need to determine factors that predispose to susceptibility and to divert treatment from surgical to medical approaches.4,5 This switch to medical treatment will require an increased knowledge of the mechanisms for several facets of aneurysms that cover the span of initiation, progression, and rupture. In this regard, many recent publications in ATVB have provided further insight into established pathways contributing to aneurysm development such as proteolysis, inflammation, and attenuation of the medial smooth muscle cell population, and a few publications have raised the possibility of new pathways such as adipokines and mineralocorticoid signaling. This article highlights these recent publications within a brief context of the literature.Risk FactorsCigarette smoking remains the major risk factor for development and progression of AAAs.6,7 Several experimental studies have demonstrated that smoke exposure augments AAA induced in mice by either subcutaneous angiotensin II (AngII) infusion or intra-aortic elastase perfusion.8,9 However, it is unclear whether cessation of smoking impacts the development of AAAs. The study of Jin et al10 demonstrated that cessation of cigarette smoking exposure did not immediately decrease the augmentation of AAAs. This sustained effect was attributable to regulation of leukocytic metabolism. Also of note is that cigarette smoking–induced augmentation of AAAs was unaffected by deficiency of matrix metalloproteinase-9 (MMP-9), MMP-12, cathepsin-S, and neutrophil elastase. AAA formation was also not reduced by doxycycline that is considered to be an MMP inhibitor of broad specificity. Doxycycline is currently under evaluation for efficacy on human AAAs (NCT01756833).11Leukocyte-Related MechanismsHuman AAAs have many populations of infiltrated leukocytes.12 Macrophages are a major cell type infiltrating AAAs, although there have been surprisingly few studies that have determined the specific function of this cell type. Boytard et al13 determined the presence of proinflammatory macrophages, with the subtype that lacks mannose receptor expression, in the adventitia and intraluminal thrombus. The study noted the increased expression of peroxiredoxin-1 as a potential target for regulating AAA development. Another macrophage-derived molecule implicated in AAA was angiopoietin-like protein 2.14 This protein has an increased abundance in AAA tissues harvested from humans and calcium chloride–induced disease in mice.T lymphocytes accumulate in large numbers in aneurysmal tissue, but the function of these cells in the disease process has not been defined. There is a diversity of T lymphocytes accumulating in AAA tissue, including natural regulatory T lymphocytes. Deletion of natural regulatory T lymphocytes, either by CD80−/−×CD86−/− or CD28−/−, augmented AngII-induced AAAs. This was assumed to be attributable to reduction of interleukin (IL)-10, with IL-10−/− mice also being susceptible to AngII-induced AAAs.15 Mice with signal transducer and activator of transcription 3-defective T lymphocytes also had augmented AAAs in a model induced by AngII infusion and coadministration of a transforming growth factor-β neutralizing antibody.16,17 Consistent with this observation, Ju et al18 demonstrated that inhibition of signal transducer and activator of transcription 3 downregulated IL-6 secretion, resulting in a decrease of AngII-induced aortic dissections in mice. This decrease was attributed to decreased recruitment of IL-17 secreting T-helper lymphocytes. Contrary to the beneficial role of natural regulatory T lymphocytes, other T lymphocytes have detrimental effects on AngII-induced AAAs as demonstrated by enhanced CD4+ cells infiltrating augmented AAAs in AngII-infused syndecan-1–deficient mice.19Leukocytic infiltration is modulated by a large number of chemokines in different inflammatory conditions.20 Chemokine (C-C motif) ligand 5 is one of several chemokines that has an inferred role in AAAs. Iida et al21 demonstrated that a peptide inhibitor (MKEY) of the interaction of chemokine (C-C motif) ligand 5 with its receptor, chemokine (C-X-C motif) ligand 4, inhibited elastase-induced AAAs in mice. This study was an example of one of the few to determine the effect of an intervention on established AAAs. Although MKEY administration did not promote AAA regression, it attenuated aortic enlargement. IL-1β has also been proposed as an inducer of leukocyte infiltration into AAAs. Antibody-based neutralization of IL-1β effects is currently under study in a large clinical trial to determine effects on atherosclerotic diseases22 and a smaller trial to assess its efficacy in limiting the growth rate of rapidly growing small AAAs (NTC02007252). The same antibody was also used to determine effects on elastase-induced AAAs. This antibody, anakinra, was effective in reducing AAAs. These data were complimented by reduced AAAs in mice deficient in IL-1β or IL-1 receptors.23 Another cytokine that has attracted attention in aneurysms is chemokine (C-C motif) receptor 2.24 Moran et al25 demonstrated that the currently approved drug as a rapamycin inhibitor, everolimus, decreased chemokine (C-C motif) receptor 2 expression and reduced AngII-induced AAAs. In addition, another immunosuppressive drug, azathioprine, was shown by Marinkovic et al26 to decrease AngII-induced AAAs. Azathioprine reduced expression of several chemokines implicated in AAA, including chemokine (C-C motif) ligand 2 and chemokine (C-C motif) ligand 5. Reduced secretion of these chemokines was via inhibition of Rac1, a c-Jun-terminal-N-kinase, which has previously attracted considerable attention as pathways that promoted AAA regression.27The Notch signaling encompasses several receptors and ligands and is required for a wide range of activities during development. Notch1 signaling is critical for development and functions of macrophages and lymphocytes. Hans et al28 demonstrated that haploinsufficiency of Notch1 reduced AngII-induced AAAs in mice through a macrophage-based mechanism.Smooth Muscle Cell–Related MechanismsAneurysms are characterized by pathology in the medial layer in which smooth muscle cells predominate.29 Smooth muscle cell–specific deletion of low density lipoprotein receptor-related protein 1 (LRP1) has previously been demonstrated to promote aortic aneurysms.30 Muratoglu et al31 have demonstrated that LRP1 deficiency in smooth muscle cells increases tissue content of a molecule, high temperature requirement factor A1t, that regulates extracellular matrix integrity. High temperature requirement factor A1t was identified as one of the many ligands for LRP1 and hence its extracellular accumulation in the lack of an removal system.Leeper et al32 also focused on the role of smooth muscle cells in mechanisms by which the genome-wide association study identified CDKN2B tumor suppressor gene participated in aneurysms formation. They found that CDKN2B was not related to inflammatory components, but instead reduced expression of the gene led to smooth muscle apoptosis via a p53-dependent mechanism. Smooth muscle cell apoptosis was also inferred in AAA formation through increases in protein kinase C-δ.33 Mice deficient in protein kinase C-δ were resistant to calcium chloride–induced AAAs, and local repopulation of the protein in deficient mice restored the susceptibility to disease. Of greater translational potential, attenuation of protein kinase C-δ activity in established AAAs reduced further aortic expansion.Many intracellular signaling pathways have been inferred in development of aneurysms.2 This has included the diverse pathways regulated by oxidation. Catalase is an important regulator of hydrogen peroxide in determining physiological and pathological responses in smooth muscle cells.34 Parastatidis et al35 demonstrated that administration of a stabilized form of catalase decreased calcium chloride–induced AAAs in mice. The smooth muscle cell specificity of the effect was demonstrated using mice in which overexpression was restricted to this cell type by expressing the protein under the control of the myosin heavy chain-α promoter. A subsequent study by Sutliff et al36 complemented this finding by demonstrating that deficiency of polymerase δ-interacting protein 2, which also regulated hydrogen peroxide availability, decreased calcium chloride–induced AAAs in mice.ProteolysisPermanent aortic dilation is a defining characteristic of aortic aneurysms. For dilation to occur in any region of the aorta, the integrity of the extracellular matrix, specifically elastin and collagen, must be compromised by proteolysis.37 The most commonly considered classes of extracellular proteases are MMPs and cathepsins. Upregulation of protease activity is likely to involve multiple mechanisms. A potentially major regulator was identified as osteoprotegerin that was detected in a large number of human AAA biopsies and determined to correlate with tissue content of several cathepsins and MMPs.38 Further evidence of the involvement of cathepsins was provided by the recent determination that deficiency of cathepsin K attenuated AAAs provoked by intra-aortic perfusion of elastase via a coordinated action on facilitating the proteolytic activity of other enzymes.39 As noted above, a role of LRP1 in aortic pathology in mice has indicated that this protein regulates protease activity, particularly the serine protease Htr-1 (a novel ligand for LRP1) in aneurysmal tissue.31 The contribution of proteolysis was also determined by overexpression of serine protease inhibitors, protease nexin-1 and plasminogen activator inhibitor-1, respectively. Overexpression of these 2 serpins in smooth muscle cells or tissue extracts harvested from thoracic aortas resulted in protection of cellular integrity through a Sma- and Mad-related protein 2 (Smad2)-dependent mechanism.40 Conversely, many studies have demonstrated that MMP inhibition reduced aortic aneurysm initiation.41 Durand et al42 determined a novel mode of decreasing AAAs induced by elastase in rabbits by the seeding of gingival fibroblasts that actively secreted the MMP inhibitor, tissue inhibitor of matrix metalloproteinase-1.Other MediatorsHypercholesterolemia is a modest risk factor for human AAAs with relatively small literature of positive and negative associations for high low-density lipoprotein cholesterol and low high-density lipoprotein cholesterol, respectively.43 An active role of high-density lipoprotein in AAA formation was revealed by reductions of AngII-induced AAAs in apolipoprotein E–deficient mice or calcium chloride–induced AAAs in C57BL/6 mice by injection of native or recombinant high-density lipoprotein.44 This effect was attributed to regulation of extracellular signal–regulated kinase signaling, which is an example of the growing complexity of high-density lipoprotein function.45The role of carbohydrate metabolism in aneurysm formation is unclear. Although aberrant carbohydrate metabolism in diabetics is assumed to augment atherosclerosis, it confers protection to AAA development.46 Glucose metabolism was enhanced in AAAs as determined by positron emission tomography using 18F-fluorodeoxyglucose as a tracer.47 The direct role of enhanced glucose metabolism on AAA formation was demonstrated by inhibition of glycolysis attenuating AAAs in both calcium chloride and AngII models of the disease. In another study, advanced glycation end products present in the skin were positively correlated with AAAs.48AngII has been implicated in both AAAs and TAAs with antagonism of AT1 receptors as the focus of several clinical trials.49 Further experimental proof was provided for benefit in TAAs in the demonstration by Kuang et al,50 who demonstrated that ascending aortic remodeling promoted by constriction of the aortic arch was reduced by angiotensin II type 1 receptor antagonism.Novel PathwaysTwo articles from ATVB raise the role of additional pathways in aortic aneurysm formation. The first study reported that leptin was present in human AAAs, and this adipokine, when applied to periaortic fat of apolipoprotein E–deficient mice, led to medial degeneration and later aneurysm formation.51 Periaortic fat is associated with increased aortic diameter, and the role of periaortic fat and its adipokines merits further investigation. The second was the study reported by Liu et al,52,53 reporting that mineralocorticoid receptor agonists induce aneurysm formation in mice. This study noted the aneurysm-provoking effects of aldosterone that were independent of mechanisms involving AngII.SummaryDevelopment of a validated medical therapy for treatment of aneurysms remains a major unmet medical need.4,5 In response to this need, there has been an expansion in research into mechanisms of aneurysmal formation, propagation, and rupture. Currently, there are several clinical trials ongoing that primarily focus on determining the benefits of inhibiting proteolysis or the renin–angiotensin system in AAAs and TAAs.49 Initial reports provide hope that medical therapies will be validated soon in demonstrating effectiveness in reducing expansion of TAAs.54AcknowledgmentsWe appreciate the editorial assistance of Dr Hong Lu.Sources of FundingAortic aneurysm research in the Daugherty laboratory is supported by HL107319.DisclosuresNone.FootnotesCorrespondence to Alan Daugherty, PhD, DSc, Saha Cardiovascular Research Center, BBSRB Room B243, 741 South Limestone, Lexington, KY 40503–0509 (e-mail [email protected]); or Janet T. Powell, MD, PhD, Department of Cancer and Surgery, Imperial College, London W6 8RP, United Kingdom (e-mail [email protected]).References1. Nordon IM, Hinchliffe RJ, Loftus IM, Thompson MM. Pathophysiology and epidemiology of abdominal aortic aneurysms.Nat Rev Cardiol. 2011; 8:92–102.CrossrefMedlineGoogle Scholar2. Lindsay ME, Dietz HC. Lessons on the pathogenesis of aneurysm from heritable conditions.Nature. 2011; 473:308–316.CrossrefMedlineGoogle Scholar3. Greenhalgh RM, Powell JT. Endovascular repair of abdominal aortic aneurysm.N Engl J Med. 2008; 358:494–501.CrossrefMedlineGoogle Scholar4. Baxter BT, Terrin MC, Dalman RL. Medical management of small abdominal aortic aneurysms.Circulation. 2008; 117:1883–1889.LinkGoogle Scholar5. Hiratzka LF, Bakris GL, Beckman JA, et al; American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines; American Association for Thoracic Surgery; American College of Radiology; American Stroke Association; Society of Cardiovascular Anesthesiologists; Society for Cardiovascular Angiography and Interventions; Society of Interventional Radiology; Society of Thoracic Surgeons; Society for Vascular Medicine. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine.Circulation. 2010; 121:e266–e369.LinkGoogle Scholar6. Reilly MP. Tobacco-related cardiovascular diseases in the 21st century.Arterioscler Thromb Vasc Biol. 2013; 33:1458–1459.LinkGoogle Scholar7. Norman PE, Curci JA. Understanding the effects of tobacco smoke on the pathogenesis of aortic aneurysm.Arterioscler Thromb Vasc Biol. 2013; 33:1473–1477.LinkGoogle Scholar8. Bergoeing MP, Arif B, Hackmann AE, Ennis TL, Thompson RW, Curci JA. Cigarette smoking increases aortic dilatation without affecting matrix metalloproteinase-9 and -12 expression in a modified mouse model of aneurysm formation.J Vasc Surg. 2007; 45:1217–1227.CrossrefMedlineGoogle Scholar9. Stolle K, Berges A, Lietz M, Lebrun S, Wallerath T. Cigarette smoke enhances abdominal aortic aneurysm formation in angiotensin II-treated apolipoprotein E-deficient mice.Toxicol Lett. 2010; 199:403–409.CrossrefMedlineGoogle Scholar10. Jin J, Arif B, Garcia-Fernandez F, Ennis TL, Davis EC, Thompson RW, Curci JA. Novel mechanism of aortic aneurysm development in mice associated with smoking and leukocytes.Arterioscler Thromb Vasc Biol. 2012; 32:2901–2909.LinkGoogle Scholar11. Thompson RW, Baxter BT. MMP inhibition in abdominal aortic aneurysms. Rationale for a prospective randomized clinical trial.Ann N Y Acad Sci. 1999; 878:159–178.CrossrefMedlineGoogle Scholar12. Rizas KD, Ippagunta N, Tilson MD. Immune cells and molecular mediators in the pathogenesis of the abdominal aortic aneurysm.Cardiol Rev. 2009; 17:201–210.CrossrefMedlineGoogle Scholar13. Boytard L, Spear R, Chinetti-Gbaguidi G, Acosta-Martin AE, Vanhoutte J, Lamblin N, Staels B, Amouyel P, Haulon S, Pinet F. Role of proinflammatory CD68(+) mannose receptor(-) macrophages in peroxiredoxin-1 expression and in abdominal aortic aneurysms in humans.Arterioscler Thromb Vasc Biol. 2013; 33:431–438.LinkGoogle Scholar14. Tazume H, Miyata K, Tian Z, et al. Macrophage-derived angiopoietin-like protein 2 accelerates development of abdominal aortic aneurysm.Arterioscler Thromb Vasc Biol. 2012; 32:1400–1409.LinkGoogle Scholar15. Ait-Oufella H, Wang Y, Herbin O, Bourcier S, Potteaux S, Joffre J, Loyer X, Ponnuswamy P, Esposito B, Dalloz M, Laurans L, Tedgui A, Mallat Z. Natural regulatory T cells limit angiotensin II-induced aneurysm formation and rupture in mice.Arterioscler Thromb Vasc Biol. 2013; 33:2374–2379.LinkGoogle Scholar16. Romain M, Taleb S, Dalloz M, Ponnuswamy P, Esposito B, Pérez N, Wang Y, Yoshimura A, Tedgui A, Mallat Z. Overexpression of SOCS3 in T lymphocytes leads to impaired interleukin-17 production and severe aortic aneurysm formation in mice–brief report.Arterioscler Thromb Vasc Biol. 2013; 33:581–584.LinkGoogle Scholar17. Wang Y, Ait-Oufella H, Herbin O, Bonnin P, Ramkhelawon B, Taleb S, Huang J, Offenstadt G, Combadière C, Rénia L, Johnson JL, Tharaux PL, Tedgui A, Mallat Z. TGF-beta activity protects against inflammatory aortic aneurysm progression and complications in angiotensin II-infused mice.J Clin Invest. 2010; 120:422–432.CrossrefMedlineGoogle Scholar18. Ju X, Ijaz T, Sun H, Ray S, Lejeune W, Lee C, Recinos A, Guo DC, Milewicz DM, Tilton RG, Brasier AR. Interleukin-6-signal transducer and activator of transcription-3 signaling mediates aortic dissections induced by angiotensin II via the T-helper lymphocyte 17-interleukin 17 axis in C57BL/6 mice.Arterioscler Thromb Vasc Biol. 2013; 33:1612–1621.LinkGoogle Scholar19. Xiao J, Angsana J, Wen J, Smith SV, Park PW, Ford ML, Haller CA, Chaikof EL. Syndecan-1 displays a protective role in aortic aneurysm formation by modulating T cell-mediated responses.Arterioscler Thromb Vasc Biol. 2012; 32:386–396.LinkGoogle Scholar20. Golledge J. Targeting chemokines in aortic aneurysm: could this be key to a novel therapy for a common problem?Arterioscler Thromb Vasc Biol. 2013; 33:670–672.LinkGoogle Scholar21. Iida Y, Xu B, Xuan H, Glover KJ, Tanaka H, Hu X, Fujimura N, Wang W, Schultz JR, Turner CR, Dalman RL. Peptide inhibitor of CXCL4-CCL5 heterodimer formation, MKEY, inhibits experimental aortic aneurysm initiation and progression.Arterioscler Thromb Vasc Biol. 2013; 33:718–726.LinkGoogle Scholar22. Ridker PM, Thuren T, Zalewski A, Libby P. Interleukin-1β inhibition and the prevention of recurrent cardiovascular events: rationale and design of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS).Am Heart J. 2011; 162:597–605.CrossrefMedlineGoogle Scholar23. Johnston WF, Salmon M, Su G, Lu G, Stone ML, Zhao Y, Owens GK, Upchurch GR, Ailawadi G. Genetic and pharmacologic disruption of interleukin-1β signaling inhibits experimental aortic aneurysm formation.Arterioscler Thromb Vasc Biol. 2013; 33:294–304.LinkGoogle Scholar24. Daugherty A, Rateri DL, Charo IF, Owens AP, Howatt DA, Cassis LA. Angiotensin II infusion promotes ascending aortic aneurysms: attenuation by CCR2 deficiency in apoE-/-mice.Clin Sci (Lond). 2010; 118:681–689.CrossrefMedlineGoogle Scholar25. Moran CS, Jose RJ, Moxon JV, Roomberg A, Norman PE, Rush C, Körner H, Golledge J. Everolimus limits aortic aneurysm in the apolipoprotein E-deficient mouse by downregulating C-C chemokine receptor 2 positive monocytes.Arterioscler Thromb Vasc Biol. 2013; 33:814–821.LinkGoogle Scholar26. Marinkovic G, Hibender S, Hoogenboezem M, van Broekhoven A, Girigorie AF, Bleeker N, Hamers AA, Stap J, van Buul JD, de Vries CJ, de Waard V. Immunosuppressive drug azathioprine reduces aneurysm progression through inhibition of Rac1 and c-Jun-terminal-N-kinase in endothelial cells.Arterioscler Thromb Vasc Biol. 2013; 33:2380–2388.LinkGoogle Scholar27. Yoshimura K, Aoki H, Ikeda Y, Fujii K, Akiyama N, Furutani A, Hoshii Y, Tanaka N, Ricci R, Ishihara T, Esato K, Hamano K, Matsuzaki M. Regression of abdominal aortic aneurysm by inhibition of c-Jun N-terminal kinase.Nat Med.2005; 11:1330–1338.CrossrefMedlineGoogle Scholar28. Hans CP, Koenig SN, Huang N, Cheng J, Beceiro S, Guggilam A, Kuivaniemi H, Partida-Sánchez S, Garg V. Inhibition of Notch1 signaling reduces abdominal aortic aneurysm in mice by attenuating macrophage-mediated inflammation.Arterioscler Thromb Vasc Biol. 2012; 32:3012–3023.LinkGoogle Scholar29. Thompson RW, Liao S, Curci JA. Vascular smooth muscle cell apoptosis in abdominal aortic aneurysms.Coron Artery Dis. 1997; 8:623–631.CrossrefMedlineGoogle Scholar30. Boucher P, Gotthardt M, Li WP, Anderson RG, Herz J. LRP: role in vascular wall integrity and protection from atherosclerosis.Science. 2003; 300:329–332.CrossrefMedlineGoogle Scholar31. Muratoglu SC, Belgrave S, Hampton B, Migliorini M, Coksaygan T, Chen L, Mikhailenko I, Strickland DK. LRP1 protects the vasculature by regulating levels of connective tissue growth factor and HtrA1.Arterioscler Thromb Vasc Biol. 2013; 33:2137–2146.LinkGoogle Scholar32. Leeper NJ, Raiesdana A, Kojima Y, et al. Loss of CDKN2B promotes p53-dependent smooth muscle cell apoptosis and aneurysm formation.Arterioscler Thromb Vasc Biol. 2013; 33:e1–e10.LinkGoogle Scholar33. Morgan S, Yamanouchi D, Harberg C, Wang Q, Keller M, Si Y, Burlingham W, Seedial S, Lengfeld J, Liu B. Elevated protein kinase C-δ contributes to aneurysm pathogenesis through stimulation of apoptosis and inflammatory signaling.Arterioscler Thromb Vasc Biol. 2012; 32:2493–2502.LinkGoogle Scholar34. Mehta PK, Griendling KK. Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system.Am J Physiol Cell Physiol. 2007; 292:C82–C97.CrossrefMedlineGoogle Scholar35. Parastatidis I, Weiss D, Joseph G, Taylor WR. Overexpression of catalase in vascular smooth muscle cells prevents the formation of abdominal aortic aneurysms.Arterioscler Thromb Vasc Biol. 2013; 33:2389–2396.LinkGoogle Scholar36. Sutliff RL, Hilenski LL, Amanso AM, Parastatidis I, Dikalova AE, Hansen L, Datla SR, Long JS, El-Ali AM, Joseph G, Gleason RL, Taylor WR, Hart CM, Griendling KK, Lassègue B. Polymerase delta interacting protein 2 sustains vascular structure and function.Arterioscler Thromb Vasc Biol. 2013; 33:2154–2161.LinkGoogle Scholar37. Brady AR, Thompson SG, Fowkes FG, Greenhalgh RM, Powell JT. Abdominal aortic aneurysm expansion. Risk factors and time intervals for surveillance.Circulation. 2004; 110:16–21.LinkGoogle Scholar38. Koole D, Hurks R, Schoneveld A, Vink A, Golledge J, Moran CS, de Kleijn DP, van Herwaarden JA, de Vries JP, Laman JD, Huizinga R, Pasterkamp G, Moll FL. Osteoprotegerin is associated with aneurysm diameter and proteolysis in abdominal aortic aneurysm disease.Arterioscler Thromb Vasc Biol. 2012; 32:1497–1504.LinkGoogle Scholar39. Sun J, Sukhova GK, Zhang J, Chen H, Sjöberg S, Libby P, Xia M, Xiong N, Gelb BD, Shi GP. Cathepsin K deficiency reduces elastase perfusion-induced abdominal aortic aneurysms in mice.Arterioscler Thromb Vasc Biol. 2012; 32:15–23.LinkGoogle Scholar40. Gomez D, Kessler K, Borges LF, Richard B, Touat Z, Ollivier V, Mansilla S, Bouton MC, Alkoder S, Nataf P, Jandrot-Perrus M, Jondeau G, Vranckx R, Michel JB. Smad2-dependent protease nexin-1 overexpression differentiates chronic aneurysms from acute dissections of human ascending aorta.Arterioscler Thromb Vasc Biol. 2013; 33:2222–2232.LinkGoogle Scholar41. Newby AC. Matrix metalloproteinase inhibition therapy for vascular diseases.Vascul Pharmacol. 2012; 56:232–244.CrossrefMedlineGoogle Scholar42. Durand E, Fournier B, Couty L, Lemitre M, Achouh P, Julia P, Trinquart L, Fabiani JN, Seguier S, Gogly B, Coulomb B, Lafont A. Endoluminal gingival fibroblast transfer reduces the size of rabbit carotid aneurisms via elastin repair.Arterioscler Thromb Vasc Biol. 2012; 32:1892–1901.LinkGoogle Scholar43. Lederle FA, Johnson GR, Wilson SE, Chute EP, Littooy FN, Bandyk D, Krupski WC, Barone GW, Acher CW, Ballard DJ. Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group.Ann Intern Med. 1997; 126:441–449.CrossrefMedlineGoogle Scholar44. Torsney E, Pirianov G, Charolidi N, Shoreim A, Gaze D, Petrova S, Laing K, Meisinger T, Xiong W, Baxter BT, Cockerill GW. Elevation of plasma high-density lipoproteins inhibits development of experimental abdominal aortic aneurysms.Arterioscler Thromb Vasc Biol. 2012; 32:2678–2686.LinkGoogle Scholar45. Rosenson RS, Brewer HB, Ansell B, Barter P, Chapman MJ, Heinecke JW, Kontush A, Tall AR, Webb NR. Translation of high-density lipoprotein function into clinical practice: current prospects and future challenges.Circulation. 2013; 128:1256–1267.LinkGoogle Scholar46. Torsney E, Pirianov G, Cockerill GW. Diabetes as a negative risk factor for abdominal aortic aneurysm - does the disease aetiology or the treatment provide the mechanism of protection?Curr Vasc Pharmacol. 2013; 11:293–298.CrossrefMedlineGoogle Scholar47. Tsuruda T, Hatakeyama K, Nagamachi S, Sekita Y, Sakamoto S, Endo GJ, Nishimura M, Matsuyama M, Yoshimura K, Sato Y, Onitsuka T, Imamura T, Asada Y, Kitamura K. Inhibition of development of abdominal aortic aneurysm by glycolysis restriction.Arterioscler Thromb Vasc Biol. 2012; 32:1410–1417.LinkGoogle Scholar48. de Vos LC, Noordzij MJ, Mulder DJ, Smit AJ, Lutgers HL, Dullaart RP, Kamphuisen PW, Zeebregts CJ, Lefrandt JD. Skin autofluorescence as a measure of advanced glycation end products deposition is elevated in peripheral artery disease.Arterioscler Thromb Vasc Biol. 2013; 33:131–138.LinkGoogle Scholar49. Moltzer E, Essers J, van Esch JH, Roos-Hesselink JW, Danser AH. The role of the renin-angiotensin system in thoracic aortic aneurysms: clinical implications.Pharmacol Ther. 2011; 131:50–60.CrossrefMedlineGoogle Scholar50. Kuang SQ, Geng L, Prakash SK, Cao JM, Guo S, Villamizar C, Kwartler CS, Peters AM, Brasier AR, Milewicz DM. Aortic remodeling after transverse aortic constriction in mice is attenuated with AT1 receptor blockade.Arterioscler Thromb Vasc Biol. 2013; 33:2172–2179.LinkGoogle Scholar51. Tao M, Yu P, Nguyen BT, Mizrahi B, Savion N, Kolodgie FD, Virmani R, Hao S, Ozaki CK, Schneiderman J. Locally applied leptin induces regional aortic wall degeneration preceding aneurysm formation in apolipoprotein E-deficient mice.Arterioscler Thromb Vasc Biol. 2013; 33:311–320.LinkGoogle Scholar52. Liu S, Xie Z, Daugherty A, Cassis LA, Pearson KJ, Gong MC, Guo Z. Mineralocorticoid receptor agonists induce mouse aortic aneurysm formation and rupture in the presence of high salt.Arterioscler Thromb Vasc Biol. 2013; 33:1568–1579.LinkGoogle Scholar53. Golledge J. Is there a new target in the renin-angiotensin system for aortic aneurysm therapy?Arterioscler Thromb Vasc Biol. 2013; 33:1456–1457.LinkGoogle Scholar54. Groenink M, den Hartog AW, Franken R, Radonic T, de Waard V, Timmermans J, Scholte AJ, van den Berg MP, Spijkerboer AM, Marquering HA, Zwinderman AH, Mulder BJ. Losartan reduces aortic dilatation rate in adults with Marfan syndrome: a randomized controlled trial.Eur Heart J. 2013; 34:3491–3500.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByShridas P, Ji A, Trumbauer A, Noffsinger V, Leung S, Dugan A, Thatcher S, Cassis L, de Beer F, Webb N and Tannock L (2022) Adipocyte-Derived Serum Amyloid A Promotes Angiotensin II–Induced Abdominal Aortic Aneurysms in Obese C57BL/6J Mice, Arteriosclerosis, Thrombosis, and Vascular Biology, 42:5, (632-643), Online publication date: 1-May-2022.Ghaghada K, Ren P, Devkota L, Starosolski Z, Zhang C, Vela D, Stupin I, Tanifum E, Annapragada A, Shen Y and LeMaire S (2021) Early Detection of Aortic Degeneration in a Mouse Model of Sporadic Aortic Aneurysm and Dissection Using Nanoparticle Contrast-Enhanced Computed Tomography, Arteriosclerosis, Thrombosis, and Vascular Biology, 41:4, (1534-1548), Online publication date: 1-Apr-2021. He J, Li N, Fan Y, Zhao X, Liu C and Hu X (2021) Metformin Inhibits Abdominal Aortic Aneurysm Formation through the Activation of the AMPK/mTOR Signaling Pathway, Journal of Vascular Research, 10.1159/000513465, 58:3, (148-158), . Dalman R, Lu Y, Mahaffey K, Chase A, Stern J and Chang R (2020) Background and Proposed Design for a Metformin Abdominal Aortic Aneurysm Suppression Trial, Vascular and Endovascular Review, 10.15420/ver.2020.03, 3 Suehiro C, Suzuki J, Hamaguchi M, Takahashi K, Nagao T, Sakaue T, Uetani T, Aono J, Ikeda S, Okura T, Okamura H and Yamaguchi O (2019) Deletion of interleukin-18 attenuates abdominal aortic aneurysm formation, Atherosclerosis, 10.1016/j.atherosclerosis.2019.08.003, 289, (14-20), Online publication date: 1-Oct-2019. Li T, Jing J, Sun L, Jiang B, Xin S, Yang J and Yuan Y (2019) TLR4 and MMP2 polymorphisms and their associations with cardiovascular risk factors in susceptibility to aortic aneurysmal diseases, Bioscience Reports, 10.1042/BSR20181591, 39:1, Online publication date: 31-Jan-2019. Wang J, Zhou Y, Wu S, Huang K, Thapa S, Tao L, Wang J, Shen Y, Wang J, Xue Y and Ji K (2018) Astragaloside IV Attenuated 3,4-Benzopyrene-Induced Abdominal Aortic Aneurysm by Ameliorating Macrophage-Mediated Inflammation, Frontiers in Pharmacology, 10.3389/fphar.2018.00496, 9 Poduri A (2018) Cellular Mechanisms of Ascending Aortic Aneurysms New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation, 10.1016/B978-0-12-809979-7.00006-7, (79-84), . Yang L, Shen L, Gao P, Li G, He Y, Wang M, Zhou H, Yuan H, Jin X and Wu X (2017) Effect of AMPK signal pathway on pathogenesis of abdominal aortic aneurysms, Oncotarget, 10.18632/oncotarget.21608, 8:54, (92827-92840), Online publication date: 3-Nov-2017. Da Ros F, Carnevale R, Cifelli G, Bizzotto D, Casaburo M, Perrotta M, Carnevale L, Vinciguerra I, Fardella S, Iacobucci R, Bressan G, Braghetta P, Lembo G and Carnevale D (2017) Targeting Interleukin-1β Protects from Aortic Aneurysms Induced by Disrupted Transforming Growth Factor β Signaling, Immunity, 10.1016/j.immuni.2017.10.016, 47:5, (959-973.e9), Online publication date: 1-Nov-2017. Sakaue T, Suzuki J, Hamaguchi M, Suehiro C, Tanino A, Nagao T, Uetani T, Aono J, Nakaoka H, Kurata M, Sakaue T, Okura T, Yasugi T, Izutani H, Higaki J and Ikeda S (2017) Perivascular Adipose Tissue Angiotensin II Type 1 Receptor Promotes Vascular Inflammation and Aneurysm Formation, Hypertension, 70:4, (780-789), Online publication date: 1-Oct-2017. Miyagawa K, Ogata T, Ueyama T, Kasahara T, Nakanishi N, Naito D, Taniguchi T, Hamaoka T, Maruyama N, Nishi M, Kimura T, Yamada H, Aoki H and Matoba S (2017) Loss of MURC/Cavin-4 induces JNK and MMP-9 activity enhancement in vascular smooth muscle cells and exacerbates abdominal aortic aneurysm, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2017.04.096, 487:3, (587-593), Online publication date: 1-Jun-2017. Qin Y, Wang Y, Liu O, Jia L, Fang W, Du J and Wei Y (2017) Tauroursodeoxycholic Acid Attenuates Angiotensin II Induced Abdominal Aortic Aneurysm Formation in Apolipoprotein E-deficient Mice by Inhibiting Endoplasmic Reticulum Stress, European Journal of Vascular and Endovascular Surgery, 10.1016/j.ejvs.2016.10.026, 53:3, (337-345), Online publication date: 1-Mar-2017. Xie J, Jones T, Feng D, Cook T, Jester A, Yi R, Jawed Y, Babbey C, March K and Murphy M (2017) Human Adipose-Derived Stem Cells Suppress Elastase-Induced Murine Abdominal Aortic Inflammation and Aneurysm Expansion through Paracrine Factors, Cell Transplantation, 10.3727/096368916X692212, 26:2, (173-189), Online publication date: 1-Feb-2017. Oda T and Matsumoto K (2015) Proteomic analysis in cardiovascular research, Surgery Today, 10.1007/s00595-015-1169-4, 46:3, (285-296), Online publication date: 1-Mar-2016. Wang K, Li Y, Shi G, Tsai H, Luo C, Cheng M, Ma C, Hsu Y, Cheng T, Chang B, Lai C and Wu H (2015) Membrane-Bound Thrombomodulin Regulates Macrophage Inflammation in Abdominal Aortic Aneurysm, Arteriosclerosis, Thrombosis, and Vascular Biology, 35:11, (2412-2422), Online publication date: 1-Nov-2015. Yu H, Littlewood T and Bennett M (2015) Akt isoforms in vascular disease, Vascular Pharmacology, 10.1016/j.vph.2015.03.003, 71, (57-64), Online publication date: 1-Aug-2015. Shen M, Lee J, Basu R, Sakamuri S, Wang X, Fan D and Kassiri Z (2015) Divergent Roles of Matrix Metalloproteinase 2 in Pathogenesis of Thoracic Aortic Aneurysm, Arteriosclerosis, Thrombosis, and Vascular Biology, 35:4, (888-898), Online publication date: 1-Apr-2015. Ye S (2015) Putative targeting of matrix metalloproteinase-8 in atherosclerosis, Pharmacology & Therapeutics, 10.1016/j.pharmthera.2014.11.007, 147, (111-122), Online publication date: 1-Mar-2015. April 2014Vol 34, Issue 4 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/ATVBAHA.114.303353PMID: 24665119 Originally publishedApril 1, 2014 Keywordsleukocytesmechanismsmooth muscle cellsproteolysisaneurysmsEditorialsPDF download Advertisement SubjectsACE/Angiotensin Receptors/Renin Angiotensin SystemAnimal Models of Human DiseaseVascular Biology" @default.
• W2155347521 created "2016-06-24" @default.
• W2155347521 creator A5048078586 @default.
• W2155347521 creator A5079061954 @default.
• W2155347521 date "2014-04-01" @default.
• W2155347521 modified "2023-10-17" @default.
• W2155347521 title "Recent Highlights of ATVB" @default.
• W2155347521 cites W1973423073 @default.
• W2155347521 cites W1974692755 @default.
• W2155347521 cites W1981643799 @default.
• W2155347521 cites W1983960375 @default.
• W2155347521 cites W1985259009 @default.
• W2155347521 cites W1985407763 @default.
• W2155347521 cites W1988167553 @default.
• W2155347521 cites W2001098777 @default.
• W2155347521 cites W2001374505 @default.
• W2155347521 cites W2028232145 @default.
• W2155347521 cites W2041938961 @default.
• W2155347521 cites W2047964681 @default.
• W2155347521 cites W2049135617 @default.
• W2155347521 cites W2049806614 @default.
• W2155347521 cites W2052402508 @default.
• W2155347521 cites W2065044287 @default.
• W2155347521 cites W2067520798 @default.
• W2155347521 cites W2068407691 @default.
• W2155347521 cites W2074115529 @default.
• W2155347521 cites W2085410562 @default.
• W2155347521 cites W2093971117 @default.
• W2155347521 cites W2096488529 @default.
• W2155347521 cites W2097178761 @default.
• W2155347521 cites W2098401063 @default.
• W2155347521 cites W2098479468 @default.
• W2155347521 cites W2103494109 @default.
• W2155347521 cites W2109329928 @default.
• W2155347521 cites W2111037557 @default.
• W2155347521 cites W2113668317 @default.
• W2155347521 cites W2119927087 @default.
• W2155347521 cites W2124913297 @default.
• W2155347521 cites W2132143276 @default.
• W2155347521 cites W2134642866 @default.
• W2155347521 cites W2135742242 @default.
• W2155347521 cites W2136042646 @default.
• W2155347521 cites W2136469880 @default.
• W2155347521 cites W2137258855 @default.
• W2155347521 cites W2145676650 @default.
• W2155347521 cites W2149538915 @default.
• W2155347521 cites W2149877677 @default.
• W2155347521 cites W2152765597 @default.
• W2155347521 cites W2153065274 @default.
• W2155347521 cites W2153933706 @default.
• W2155347521 cites W2154777572 @default.
• W2155347521 cites W2155854521 @default.
• W2155347521 cites W2156835140 @default.
• W2155347521 cites W2158094210 @default.
• W2155347521 cites W2158680134 @default.
• W2155347521 cites W2161449775 @default.
• W2155347521 cites W2162313189 @default.
• W2155347521 cites W2163490310 @default.
• W2155347521 cites W2165927667 @default.
• W2155347521 cites W2167010408 @default.
• W2155347521 cites W2613454590 @default.
• W2155347521 doi "https://doi.org/10.1161/atvbaha.114.303353" @default.
• W2155347521 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24665119" @default.
• W2155347521 hasPublicationYear "2014" @default.
• W2155347521 type Work @default.
• W2155347521 sameAs 2155347521 @default.
• W2155347521 citedByCount "23" @default.
• W2155347521 countsByYear W21553475212014 @default.
• W2155347521 countsByYear W21553475212015 @default.
• W2155347521 countsByYear W21553475212017 @default.
• W2155347521 countsByYear W21553475212018 @default.
• W2155347521 countsByYear W21553475212019 @default.
• W2155347521 countsByYear W21553475212020 @default.
• W2155347521 countsByYear W21553475212021 @default.
• W2155347521 countsByYear W21553475212022 @default.
• W2155347521 countsByYear W21553475212023 @default.
• W2155347521 crossrefType "journal-article" @default.
• W2155347521 hasAuthorship W2155347521A5048078586 @default.
• W2155347521 hasAuthorship W2155347521A5079061954 @default.
• W2155347521 hasBestOaLocation W21553475211 @default.
• W2155347521 hasConcept C41008148 @default.
• W2155347521 hasConceptScore W2155347521C41008148 @default.
• W2155347521 hasIssue "4" @default.
• W2155347521 hasLocation W21553475211 @default.
• W2155347521 hasLocation W21553475212 @default.
• W2155347521 hasOpenAccess W2155347521 @default.
• W2155347521 hasPrimaryLocation W21553475211 @default.
• W2155347521 hasRelatedWork W1964848317 @default.
• W2155347521 hasRelatedWork W2029744004 @default.
• W2155347521 hasRelatedWork W2068872642 @default.
• W2155347521 hasRelatedWork W2076393078 @default.
• W2155347521 hasRelatedWork W2086120259 @default.
• W2155347521 hasRelatedWork W2086127513 @default.
• W2155347521 hasRelatedWork W2137941439 @default.
• W2155347521 hasRelatedWork W2141795027 @default.
• W2155347521 hasRelatedWork W3186982001 @default.
• W2155347521 hasRelatedWork W95829383 @default.
• W2155347521 hasVolume "34" @default.

• next