FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3048393148> ?p ?o ?g. }

• W3048393148 endingPage "L549" @default.
• W3048393148 startingPage "L547" @default.
• W3048393148 abstract "EditorialTaking it to heart: dissecting cardiopulmonary interactions in diseases of the lung and the cardiovascular systemTim LahmTim LahmDivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Indiana University School of Medicine, Indianapolis, IndianaDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IndianaRichard L. Roudebush Department of Veterans Affairs Medical Center, Indianapolis, IndianaPublished Online:04 Sep 2020https://doi.org/10.1152/ajplung.00373.2020This is the final version - click for previous versionMoreSectionsPDF (55 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat World Heart Day, celebrated annually on September 29, was established by the World Heart Federation to generate awareness of cardiovascular disease (CVD) (7). CVD truly is a global disease that affects millions of people worldwide. Although the types and manifestations of CVD differ between certain parts of the world, the various CVDs share the unfortunate feature of leading to significant morbidity and mortality. In addition, CVDs may profoundly affect the quality of life of affected individuals and make affected individuals more prone to suffering unfavorable outcomes in emerging diseases such as COVID-19 (14, 31). Not surprisingly, the public health relevance and fiscal consequences of CVDs are substantial. The impact of CVD across the world, strategies for addressing several of the major knowledge and treatment gaps, and the role of the World Heart Federation in addressing the burden of CVD are outlined eloquently in an editorial by Maarman et al. in this issue of AJP Lung (20). The authors remind us that after 20 years the importance of World Heart Day is still eminent.Although CVD without a doubt represents a major global health burden, one may wonder why a pulmonary journal such as AJP Lung is highlighting World Heart Day and why a pulmonologist is writing an accompanying editorial. The answer is easy: nearly all pulmonary diseases have the potential to affect the right side of the heart (12). This right heart involvement, which can be observed in acute as well as chronic lung disease, may either occur indirectly and subsequentially [usually as a consequence of the development of acute and/or chronic pulmonary hypertension (PH)] or concomitantly [through a pathophysiological process that targets both the lung and heart, e.g., cigarette smoke exposure, side effects of chemotherapeutics, microvascular thrombosis in sepsis, and/or acute respiratory distress syndrome (ARDS)]. In addition, several common diseases such as diabetes, hyperlipidemia, and obstructive sleep apnea induce widespread endothelial cell dysfunction and simultaneously target and affect both the lung as well as the heart (both the right and left heart). In fact, right heart abnormalities in subjects exposed to cigarette smoke may occur even before signs of lung disease are observed (27). With regard to PH development in acute or chronic lung disease, it is important to note that, no matter what the underlying lung disease is, as soon as PH and cor pulmonale develop, morbidity and mortality of affected individuals increase significantly (2, 5, 21, 25). Another interesting observation is that, although the “typical” phenotype of right heart involvement in chronic lung disease is that of an enlarged and hypertrophied right ventricle (RV) and a dilated right atrium, in a subset of patients with chronic obstructive pulmonary disease (COPD), a small and atrophied right heart has been described (11), possibly representing a process of cardiopenia that may be similar to the sarcopenia that can be seen in this patient population.On the other hand, it has long been known that any type of left heart disease can cause lung disease and right heart abnormalities (24). This typically occurs through the development of PH and subsequent right heart congestion. In addition, given the shared pericardial sac as well as shared myocardial fibers, mechanical changes associated with left heart enlargement may directly affect the geometry and mechanics of the RV, thus leading to RV dysfunction. In this context, it is worthwhile noting that the interventricular septum contributes ~40% to the RV ejection fraction (26). In addition to PH, the lung may be affected by left heart disease through the development of pulmonary edema, pleural effusions, compressive atelectasis due to left heart enlargement, or pulmonary emboli. Finally, several drugs used to treat CVD or its consequences may harm the lung and lead to alveolar hemorrhage (anticoagulants), chronic cough [angiotensin-converting enzyme (ACE) inhibitors], pulmonary fibrosis (amiodarone), or acute lung injury (amiodarone).Given the intricacies of lung-heart interactions, clinicians and researchers have coined the terms “cardiopulmonary system” and “cardiopulmonary axis.” This is why a pulmonary journal like AJP Lung indeed should pay attention to the heart and the cardiovascular system (and why cardiovascular journals, in turn, should pay attention to diseases of the lung). Given the global burden of CVD as well as respiratory diseases such as COPD, obstructive sleep apnea, and ARDS, and given the high prevalence of combined heart and lung disease throughout the world, involvement of the cardiopulmonary axis is a global issue (4). In addition, since many CVDs and respiratory diseases disproportionally affect underrepresented minorities, involvement of the cardiopulmonary axis represents a significant problem in these populations (30). It is therefore timely and relevant that AJP Lung is highlighting the importance of World Heart Day in this issue.In addition to highlighting World Heart Day, AJP Lung has addressed the role of cardiopulmonary interactions by publishing several insightful and thought-provoking articles investigating the role of the right heart and cardiopulmonary interaction in various pulmonary conditions or respiratory exposures. These articles center on a variety of topics such as sex differences and estrogen signaling in RV function in PH (9, 18); effects of perinatal hyperoxia or hypoxia on RV function later in life (10, 15); effects of HIV, opioids, or vaping on endothelial function and cardiorespiratory parameters (1, 3); bone morphogenetic protein receptor 2 (BMPR2) regulation of insulin and glucose signaling in cardiomyocytes (13); interdependence of RV glucose uptake, hypoxia and β-adrenergic receptor signaling in PH (28); effects of pulmonary vascular thrombospondin 1/CD47 signaling on RV afterload in sickle cell disease (22); differences in mesothelial mobilization between the developing lung and heart (19); and effects of episodic hypercapnic stimulation on respiratory-cardiovascular coupling in volume-overload heart failure (6). Two studies assessed the effects of established treatments for pulmonary arterial hypertension (PAH; used in combination with other established or emerging PAH treatments) on RV adaptation, using novel end points or novel delivery methods (16, 23). A review article focused on the role of angiogenesis in the development of right heart failure in PH (8). A review in AJP Lung’s sister journal Physiology discussed physiological aspects of RV-pulmonary vascular interactions (29). In conglomerate, these studies and reviews demonstrate tight interactions between the respiratory and cardiovascular systems and reveal that several exposures, environmental stimuli, and intrinsic factors previously thought to only affect the lung actually engage pathways that are active in both organ systems. In addition, several of the abovementioned studies revealed that cardiovascular adaptation in the setting of lung disease is dependent on biologically relevant factors such as sex, age, metabolism, and genetics.However, although we have learned a great deal about cardiopulmonary interactions in the setting of lung disease, several knowledge gaps remain: First, it often is difficult to dissect whether interventions shown to improve RV adaptation exert their RV-protective effects directly by targeting the RV or more indirectly by lowering RV afterload through pulmonary vascular effects. Studies employing pressure-volume loops, pulmonary artery banding models, or cultured isolated RV cardiomyocytes are needed to answer this question (17). Second, although we have just started to understand that sex/gender, age, and lifestyle factors such as exercise and diet are clinically important modifiers of cardiopulmonary interactions, more studies are needed to understand the underlying mechanisms (17). This, in turn, may allow for the development of novel, personalized treatment strategies aimed at improving cardiopulmonary adaptations in chronic lung and/or heart diseases. Along those lines, race and socioeconomic factors are significant disease modifiers in both the cardiovascular system and the lung, and their effects on the cardiopulmonary axis need to be studied in more detail (30). Third, although it is well known that many interventions in chronic lung or cardiovascular disease improve respiratory or cardiovascular function, respectively, effects of novel respiratory interventions on the cardiovascular system (and vice versa) need to be studied in more detail. Finally, given the current COVID-19 pandemic, and given the frequent lung and occasional heart involvement in this disease (14, 31), it is imperative that we better understand short-term as well as long-term cardiopulmonary complications of and cardiopulmonary interactions in SARS-CoV-2 infection.Importantly, all these knowledge gaps have significant global implications that must not be neglected. Addressing these gaps therefore should involve a coordinated global effort, so that results from basic, translational, and clinical studies are maximally generalizable. Multicountry organizations such as the World Heart Federation and the Pulmonary Vascular Research Institute have the resources and wherewithal to lead global efforts in the fight against cardiopulmonary disease (4, 20). In fact, both organizations have made major contributions in this field by 1) supporting research, education, and clinical care, 2) establishing international working groups and facilitating multicountry collaborations, 3) providing training programs, 4) pursuing advocacy and public outreach, and 5) establishing global registries.In summary, diseases of the lung or the cardiovascular system should not be looked at in isolation. An integrative approach that encompasses assessing effects of exposures and interventions on the entire cardiopulmonary axis is likely to maximize scientific insight and enhance clinical responses. World Heart Day reminds us that pulmonologists and researchers studying the respiratory system should worry about the heart and that CVD specialists and researchers should pay attention to the lung. Addressing the cardiopulmonary system as a whole, ideally while leveraging the power of the exciting -omics, genetic, and phenotyping tools that are currently available, will facilitate the development of novel, personalized pharmacological and nonpharmacological interventions that are safe, efficacious, and equitable.GRANTSThis work was supported by Department of Veterans Affairs Merit Review Award 2 I01 BX002042-06 (T.L.) and National Heart, Lung, and Blood Institute Grant HL144727-01A1 (T.L.).DISCLOSUREST.L. received consulting fees from Bayer and research reagents from Eli Lilly & Company.AUTHOR CONTRIBUTIONST.L. drafted manuscript; edited and revised manuscript; and approved final version of manuscript.REFERENCES1. Agarwal S, Sharma H, Chen L, Dhillon NK. NADPH oxidase-mediated endothelial injury in HIV- and opioid-induced pulmonary arterial hypertension. Am J Physiol Lung Cell Mol Physiol 318: L1097–L1108, 2020. doi:10.1152/ajplung.00480.2019. Link | ISI | Google Scholar2. Boerrigter BG, Bogaard HJ, Trip P, Groepenhoff H, Rietema H, Holverda S, Boonstra A, Postmus PE, Westerhof N, Vonk-Noordegraaf A. Ventilatory and cardiocirculatory exercise profiles in COPD: the role of pulmonary hypertension. Chest 142: 1166–1174, 2012. doi:10.1378/chest.11-2798. Crossref | PubMed | ISI | Google Scholar3. Chaumont M, Tagliatti V, Channan EM, Colet JM, Bernard A, Morra S, Deprez G, Van Muylem A, Debbas N, Schaefer T, Faoro V, van de Borne P. Short halt in vaping modifies cardiorespiratory parameters and urine metabolome: a randomized trial. Am J Physiol Lung Cell Mol Physiol 318: L331–L344, 2020. doi:10.1152/ajplung.00268.2019. Link | ISI | Google Scholar4. Corris PA, Seeger W. Call it by the correct name—pulmonary hypertension not pulmonary arterial hypertension: growing recognition of the global health impact for a well-recognized condition and the role of the Pulmonary Vascular Research Institute. Am J Physiol Lung Cell Mol Physiol 318: L992–L994, 2020. doi:10.1152/ajplung.00098.2020. Link | ISI | Google Scholar5. Cottin V, Le Pavec J, Prévot G, Mal H, Humbert M, Simonneau G, Cordier JF; GERM“O”P. Pulmonary hypertension in patients with combined pulmonary fibrosis and emphysema syndrome. Eur Respir J 35: 105–111, 2010. doi:10.1183/09031936.00038709. Crossref | PubMed | ISI | Google Scholar6. Díaz HS, Andrade DC, Toledo C, Pereyra KV, Schwarz KG, Díaz-Jara E, Lucero C, Arce-Álvarez A, Schultz HD, Silva JN, Takakura AC, Moreira TS, Marcus NJ, Del Rio R. Episodic stimulation of central chemoreceptor neurons elicits disordered breathing and autonomic dysfunction in volume overload heart failure. Am J Physiol Lung Cell Mol Physiol 318: L27–L40, 2020. doi:10.1152/ajplung.00007.2019. Link | ISI | Google Scholar7. World Heath Federation. Leading the global fight against CVD (Online). https://www.world-heart-federation.org/about-us/who-we-are/ [3 August 2020].Google Scholar8. Frump AL, Bonnet S, de Jesus Perez VA, Lahm T. Emerging role of angiogenesis in adaptive and maladaptive right ventricular remodeling in pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol 314: L443–L460, 2018. doi:10.1152/ajplung.00374.2017. Link | ISI | Google Scholar9. Frump AL, Goss KN, Vayl A, Albrecht M, Fisher A, Tursunova R, Fierst J, Whitson J, Cucci AR, Brown MB, Lahm T. Estradiol improves right ventricular function in rats with severe angioproliferative pulmonary hypertension: effects of endogenous and exogenous sex hormones. Am J Physiol Lung Cell Mol Physiol 308: L873–L890, 2015. doi:10.1152/ajplung.00006.2015. Link | ISI | Google Scholar10. Goss KN, Cucci AR, Fisher AJ, Albrecht M, Frump A, Tursunova R, Gao Y, Brown MB, Petrache I, Tepper RS, Ahlfeld SK, Lahm T. Neonatal hyperoxic lung injury favorably alters adult right ventricular remodeling response to chronic hypoxia exposure. Am J Physiol Lung Cell Mol Physiol 308: L797–L806, 2015. doi:10.1152/ajplung.00276.2014. Link | ISI | Google Scholar11. Grau M, Barr RG, Lima JA, Hoffman EA, Bluemke DA, Carr JJ, Chahal H, Enright PL, Jain A, Prince MR, Kawut SM. Percent emphysema and right ventricular structure and function: the Multi-Ethnic Study of Atherosclerosis-Lung and Multi-Ethnic Study of Atherosclerosis-Right Ventricle Studies. Chest 144: 136–144, 2013. doi:10.1378/chest.12-1779. Crossref | PubMed | ISI | Google Scholar12. Han MK, McLaughlin VV, Criner GJ, Martinez FJ. Pulmonary diseases and the heart. Circulation 116: 2992–3005, 2007. doi:10.1161/CIRCULATIONAHA.106.685206. Crossref | PubMed | ISI | Google Scholar13. Hemnes AR, Fessel JP, Chen X, Zhu S, Fortune NL, Jetter C, Freeman M, Newman JH, West JD, Talati MH. BMPR2 dysfunction impairs insulin signaling and glucose homeostasis in cardiomyocytes. Am J Physiol Lung Cell Mol Physiol 318: L429–L441, 2020. doi:10.1152/ajplung.00555.2018. Link | ISI | Google Scholar14. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, Zhang L, Fan G, Xu J, Gu X, Cheng Z, Yu T, Xia J, Wei Y, Wu W, Xie X, Yin W, Li H, Liu M, Xiao Y, Gao H, Guo L, Xie J, Wang G, Jiang R, Gao Z, Jin Q, Wang J, Cao B. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 395: 497–506, 2020. doi:10.1016/S0140-6736(20)30183-5. Crossref | PubMed | ISI | Google Scholar15. Krishnan S, Stearman RS, Zeng L, Fisher A, Mickler EA, Rodriguez BH, Simpson ER, Cook T, Slaven JE, Ivan M, Geraci MW, Lahm T, Tepper RS. Transcriptomic modifications in developmental cardiopulmonary adaptations to chronic hypoxia using a murine model of simulated high-altitude exposure. Am J Physiol Lung Cell Mol Physiol. In press. doi:10.1152/ajplung.00487.2019. Link | Google Scholar16. Lachant DJ, Meoli DF, Haight D, Staicu S, Akers S, Glickman S, Ambrosini R, Champion HC, White RJ. Combination therapy improves vascular volume in female rats with pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol 317: L445–L455, 2019. doi:10.1152/ajplung.00450.2018. Link | ISI | Google Scholar17. Lahm T, Douglas IS, Archer SL, Bogaard HJ, Chesler NC, Haddad F, Hemnes AR, Kawut SM, Kline JA, Kolb TM, Mathai SC, Mercier O, Michelakis ED, Naeije R, Tuder RM, Ventetuolo CE, Vieillard-Baron A, Voelkel NF, Vonk-Noordegraaf A, Hassoun PM; American Thoracic Society Assembly on Pulmonary Circulation. Assessment of right ventricular function in the research setting: knowledge gaps and pathways forward. An official American Thoracic Society Research Statement. Am J Respir Crit Care Med 198: e15–e43, 2018. doi:10.1164/rccm.201806-1160ST. Crossref | PubMed | ISI | Google Scholar18. Lahm T, Frump AL, Albrecht ME, Fisher AJ, Cook TG, Jones TJ, Yakubov B, Whitson J, Fuchs RK, Liu A, Chesler NC, Brown MB. 17β-Estradiol mediates superior adaptation of right ventricular function to acute strenuous exercise in female rats with severe pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol 311: L375–L388, 2016. doi:10.1152/ajplung.00132.2016. Link | ISI | Google Scholar19. Lüdtke TH, Rudat C, Kurz J, Häfner R, Greulich F, Wojahn I, Aydoğdu N, Mamo TM, Kleppa MJ, Trowe MO, Bohnenpoll T, Taketo MM, Kispert A. Mesothelial mobilization in the developing lung and heart differs in timing, quantity, and pathway dependency. Am J Physiol Lung Cell Mol Physiol 316: L767–L783, 2019. doi:10.1152/ajplung.00212.2018. Link | ISI | Google Scholar20. Maarman GJ, Chakafana G, Sliwa K. World Heart Day: a World Heart Federation communiqué on the future of basic sciences and translational medicine in global cardiovascular research. Am J Physiol Lung Cell Mol Physiol. In press. doi:10.1152/ajplung.00339.2020. Link | Google Scholar21. Mekontso Dessap A, Boissier F, Charron C, Bégot E, Repessé X, Legras A, Brun-Buisson C, Vignon P, Vieillard-Baron A. Acute cor pulmonale during protective ventilation for acute respiratory distress syndrome: prevalence, predictors, and clinical impact. Intensive Care Med 42: 862–870, 2016. doi:10.1007/s00134-015-4141-2. Crossref | PubMed | ISI | Google Scholar22. Novelli EM, Little-Ihrig L, Knupp HE, Rogers NM, Yao M, Baust JJ, Meijles D, St Croix CM, Ross MA, Pagano PJ, DeVallance ER, Miles G, Potoka KP, Isenberg JS, Gladwin MT. Vascular TSP1-CD47 signaling promotes sickle cell-associated arterial vasculopathy and pulmonary hypertension in mice. Am J Physiol Lung Cell Mol Physiol 316: L1150–L1164, 2019. doi:10.1152/ajplung.00302.2018. Link | ISI | Google Scholar23. Rashid J, Nozik-Grayck E, McMurtry IF, Stenmark KR, Ahsan F. Inhaled combination of sildenafil and rosiglitazone improves pulmonary hemodynamics, cardiac function, and arterial remodeling. Am J Physiol Lung Cell Mol Physiol 316: L119–L130, 2019. doi:10.1152/ajplung.00381.2018. Link | ISI | Google Scholar24. Remetz MS, Cleman MW, Cabin HS. Pulmonary and pleural complications of cardiac disease. Clin Chest Med 10: 545–592, 1989. Crossref | PubMed | ISI | Google Scholar25. Rivera-Lebron BN, Forfia PR, Kreider M, Lee JC, Holmes JH, Kawut SM. Echocardiographic and hemodynamic predictors of mortality in idiopathic pulmonary fibrosis. Chest 144: 564–570, 2013. doi:10.1378/chest.12-2298. Crossref | PubMed | ISI | Google Scholar26. Santamore WP, Dell’Italia LJ. Ventricular interdependence: significant left ventricular contributions to right ventricular systolic function. Prog Cardiovasc Dis 40: 289–308, 1998. doi:10.1016/S0033-0620(98)80049-2. Crossref | PubMed | ISI | Google Scholar27. Seimetz M, Parajuli N, Pichl A, Veit F, Kwapiszewska G, Weisel FC, Milger K, Egemnazarov B, Turowska A, Fuchs B, Nikam S, Roth M, Sydykov A, Medebach T, Klepetko W, Jaksch P, Dumitrascu R, Garn H, Voswinckel R, Kostin S, Seeger W, Schermuly RT, Grimminger F, Ghofrani HA, Weissmann N. Inducible NOS inhibition reverses tobacco-smoke-induced emphysema and pulmonary hypertension in mice. Cell 147: 293–305, 2011. doi:10.1016/j.cell.2011.08.035. Crossref | PubMed | ISI | Google Scholar28. Stephens OR, Weiss K, Frimel M, Rose JA, Sun Y, Asosingh K, Farha S, Highland KB, Prasad SV, Erzurum SC. Interdependence of hypoxia and β-adrenergic receptor signaling in pulmonary arterial hypertension. Am J Physiol Lung Cell Mol Physiol 317: L369–L380, 2019. doi:10.1152/ajplung.00015.2019. Link | ISI | Google Scholar29. Tabima DM, Philip JL, Chesler NC. Right ventricular-pulmonary vascular interactions. Physiology (Bethesda) 32: 346–356, 2017. doi:10.1152/physiol.00040.2016. Link | ISI | Google Scholar30. Talwar A, Garcia JG, Tsai H, Moreno M, Lahm T, Zamanian RT, Machado R, Kawut SM, Selej M, Mathai S, D’Anna LH, Sahni S, Rodriquez EJ, Channick R, Fagan K, Gray M, Armstrong J, Rodriguez Lopez J, de Jesus Perez V; Pulmonary Circulation Assembly. Health disparities in patients with pulmonary arterial hypertension: a blueprint for action. An official American Thoracic Society Statement. Am J Respir Crit Care Med 196: e32–e47, 2017. doi:10.1164/rccm.201709-1821ST. Crossref | PubMed | ISI | Google Scholar31. Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, Xiang J, Wang Y, Song B, Gu X, Guan L, Wei Y, Li H, Wu X, Xu J, Tu S, Zhang Y, Chen H, Cao B. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet 395: 1054–1062, 2020. doi:10.1016/S0140-6736(20)30566-3. Crossref | PubMed | ISI | Google ScholarAUTHOR NOTESCorrespondence: T. Lahm ([email protected]edu). Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Related ArticlesWorld health observances in September 2020: sepsis, the lung and heart, and pulmonary fibrosis in focus 04 Sep 2020American Journal of Physiology-Lung Cellular and Molecular PhysiologyWorld Heart Day: a World Heart Federation communiqué on the future of basic sciences and translational medicine in global cardiovascular research 04 Sep 2020American Journal of Physiology-Lung Cellular and Molecular PhysiologyCited ByAn American Physiological Society cross-journal Call for Papers on “Inter-Organ Communication in Homeostasis and Disease”Sue C. Bodine, Heddwen L. Brooks, Nigel W. Bunnett, Hilary A. Coller, Mark R. Frey, Bina Joe, Thomas R. Kleyman, Merry L. Lindsey, André Marette, Rory E. Morty, Jan-Marino Ramírez, Morten B. Thomsen, and Gina L. C. Yosten28 June 2021 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 321, No. 1World health observances in September 2020: sepsis, the lung and heart, and pulmonary fibrosis in focusClaudio Nardiello and Rory E. Morty4 September 2020 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 319, No. 3 More from this issue > Volume 319Issue 3September 2020Pages L547-L549 https://doi.org/10.1152/ajplung.00373.2020PubMed32783622History Received 4 August 2020 Accepted 4 August 2020 Published online 4 September 2020 Published in print 1 September 2020 Keywordscardiopulmonary axiscor pulmonaleleft heart diseaselung diseasepulmonary hypertension Metrics" @default.
• W3048393148 created "2020-08-18" @default.
• W3048393148 creator A5042912090 @default.
• W3048393148 date "2020-09-01" @default.
• W3048393148 modified "2023-09-26" @default.
• W3048393148 title "Taking it to heart: dissecting cardiopulmonary interactions in diseases of the lung and the cardiovascular system" @default.
• W3048393148 cites W2038311789 @default.
• W3048393148 cites W2039169978 @default.
• W3048393148 cites W2108221622 @default.
• W3048393148 cites W2118645906 @default.
• W3048393148 cites W2125619852 @default.
• W3048393148 cites W2126162698 @default.
• W3048393148 cites W2132798299 @default.
• W3048393148 cites W2143099536 @default.
• W3048393148 cites W2171190332 @default.
• W3048393148 cites W2208635741 @default.
• W3048393148 cites W2346145848 @default.
• W3048393148 cites W2417409779 @default.
• W3048393148 cites W2748324785 @default.
• W3048393148 cites W2760979132 @default.
• W3048393148 cites W2765352371 @default.
• W3048393148 cites W2886383171 @default.
• W3048393148 cites W2897515021 @default.
• W3048393148 cites W2913120527 @default.
• W3048393148 cites W2922716216 @default.
• W3048393148 cites W2955902429 @default.
• W3048393148 cites W2964282382 @default.
• W3048393148 cites W2981183735 @default.
• W3048393148 cites W2987515801 @default.
• W3048393148 cites W2995992021 @default.
• W3048393148 cites W3001118548 @default.
• W3048393148 cites W3009885589 @default.
• W3048393148 cites W3014850916 @default.
• W3048393148 cites W3014901372 @default.
• W3048393148 cites W3040861926 @default.
• W3048393148 cites W3045756644 @default.
• W3048393148 doi "https://doi.org/10.1152/ajplung.00373.2020" @default.
• W3048393148 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7518052" @default.
• W3048393148 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32783622" @default.
• W3048393148 hasPublicationYear "2020" @default.
• W3048393148 type Work @default.
• W3048393148 sameAs 3048393148 @default.
• W3048393148 citedByCount "3" @default.
• W3048393148 countsByYear W30483931482020 @default.
• W3048393148 countsByYear W30483931482021 @default.
• W3048393148 countsByYear W30483931482023 @default.
• W3048393148 crossrefType "journal-article" @default.
• W3048393148 hasAuthorship W3048393148A5042912090 @default.
• W3048393148 hasBestOaLocation W30483931481 @default.
• W3048393148 hasConcept C126322002 @default.
• W3048393148 hasConcept C164705383 @default.
• W3048393148 hasConcept C177713679 @default.
• W3048393148 hasConcept C2777714996 @default.
• W3048393148 hasConcept C71924100 @default.
• W3048393148 hasConceptScore W3048393148C126322002 @default.
• W3048393148 hasConceptScore W3048393148C164705383 @default.
• W3048393148 hasConceptScore W3048393148C177713679 @default.
• W3048393148 hasConceptScore W3048393148C2777714996 @default.
• W3048393148 hasConceptScore W3048393148C71924100 @default.
• W3048393148 hasFunder F4320306127 @default.
• W3048393148 hasFunder F4320337338 @default.
• W3048393148 hasIssue "3" @default.
• W3048393148 hasLocation W30483931481 @default.
• W3048393148 hasLocation W30483931482 @default.
• W3048393148 hasLocation W30483931483 @default.
• W3048393148 hasOpenAccess W3048393148 @default.
• W3048393148 hasPrimaryLocation W30483931481 @default.
• W3048393148 hasRelatedWork W2008851126 @default.
• W3048393148 hasRelatedWork W2011347913 @default.
• W3048393148 hasRelatedWork W2049397185 @default.
• W3048393148 hasRelatedWork W2073151595 @default.
• W3048393148 hasRelatedWork W2074833529 @default.
• W3048393148 hasRelatedWork W2125804349 @default.
• W3048393148 hasRelatedWork W2159512267 @default.
• W3048393148 hasRelatedWork W2304633692 @default.
• W3048393148 hasRelatedWork W2355498105 @default.
• W3048393148 hasRelatedWork W2399063111 @default.
• W3048393148 hasVolume "319" @default.
• W3048393148 isParatext "false" @default.
• W3048393148 isRetracted "false" @default.
• W3048393148 magId "3048393148" @default.
• W3048393148 workType "article" @default.