FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2912477387> ?p ?o ?g. }

• W2912477387 endingPage "688" @default.
• W2912477387 startingPage "688" @default.
• W2912477387 abstract "The emerging roles of MMPs in the pathogenesis of different forms of cardiovascular disease has garnered increased attention from researchers in both clinical and basic sciences during the past decade. Fibrillar collagen, ie types I and III, confer tensile strength to tissues, and these proteins are constitutively expressed by specific nonmyocyte cells in heart and valves. Healthy cardiac valves depend upon ongoing collagen turnover (mediated by cardiac myofibroblasts) for maintenance of normal tissue structure and function. This phenomenon represents a balance struck between fibrillar collagen deposition and its removal by specific MMPs synthesized by myofibroblasts in the valve. Furthermore, the significance of TIMPs in inhibiting endogenous MMP activity in healthy and diseased myocardium is now generally acknowledged. Nonrheumatic aortic stenosis (NAS) is attended by a host of alterations including the genesis of fibrocalcific masses and loss of normal valvular geometry, ie thickening. These alterations are associated with the loss of passive mechanical and elastic properties of these tissues which are associated with the development of stenosis. In the setting of NAS, inflammatory responses and inappropriate collagen remodeling in valves are akin to those observed in other cardiac fibrotic disorders, including wound healing observed after large myocardial infarction. Despite the current repertoire of surgical interventions available to correct aortic stenosis, the mechanisms underlying the pathogenesis of this disease are not well understood. While many cardiac fibroproliferative disorders are marked by excessive collagen synthesis and deposition in response to abnormal cytokine, mechanical stretch, and neurohormonal inputs, the current paper by Satta and colleagues provides evidence to support the hypothesis that persistent MMP-9 activation in the calcified valve is implicated in stenosis. The most striking contribution of the current work is the suggestion that abnormal MMP activation may due to a lack of sufficient inhibition provided by endogenous tissue TIMPs in the diseased valves. These findings are of considerable clinical interest and provide the basis for a novel mechanism for the development of NAS. The strong positive correlation between MMP-9 activity and the downregulation of TIMP function in valvular tissues is an attractive hypothesis; the current results are exciting developments insofar as they may provide a target on which to focus eventual therapeutic intervention, and this confers considerable promise for further investigation. An improved understanding of endogenous maladaptive changes within the stenotic valves may provide the basis for genetic or pharmacologic manipulation of TIMP expression or activity, respectively, in delaying the onset of chronic aortic stenosis." @default.
• W2912477387 created "2019-02-21" @default.
• W2912477387 creator A5013475148 @default.
• W2912477387 creator A5037459846 @default.
• W2912477387 date "2003-09-01" @default.
• W2912477387 modified "2023-09-25" @default.
• W2912477387 title "Invited commentary" @default.
• W2912477387 doi "https://doi.org/10.1016/s0003-4975(03)00708-2" @default.
• W2912477387 hasPublicationYear "2003" @default.
• W2912477387 type Work @default.
• W2912477387 sameAs 2912477387 @default.
• W2912477387 citedByCount "0" @default.
• W2912477387 crossrefType "journal-article" @default.
• W2912477387 hasAuthorship W2912477387A5013475148 @default.
• W2912477387 hasAuthorship W2912477387A5037459846 @default.
• W2912477387 hasConcept C109523444 @default.
• W2912477387 hasConcept C126322002 @default.
• W2912477387 hasConcept C142724271 @default.
• W2912477387 hasConcept C164705383 @default.
• W2912477387 hasConcept C203014093 @default.
• W2912477387 hasConcept C207865475 @default.
• W2912477387 hasConcept C2776914184 @default.
• W2912477387 hasConcept C2779537366 @default.
• W2912477387 hasConcept C2779736815 @default.
• W2912477387 hasConcept C2780007028 @default.
• W2912477387 hasConcept C2780269544 @default.
• W2912477387 hasConcept C2780559512 @default.
• W2912477387 hasConcept C2780714102 @default.
• W2912477387 hasConcept C2780942790 @default.
• W2912477387 hasConcept C500558357 @default.
• W2912477387 hasConcept C71924100 @default.
• W2912477387 hasConceptScore W2912477387C109523444 @default.
• W2912477387 hasConceptScore W2912477387C126322002 @default.
• W2912477387 hasConceptScore W2912477387C142724271 @default.
• W2912477387 hasConceptScore W2912477387C164705383 @default.
• W2912477387 hasConceptScore W2912477387C203014093 @default.
• W2912477387 hasConceptScore W2912477387C207865475 @default.
• W2912477387 hasConceptScore W2912477387C2776914184 @default.
• W2912477387 hasConceptScore W2912477387C2779537366 @default.
• W2912477387 hasConceptScore W2912477387C2779736815 @default.
• W2912477387 hasConceptScore W2912477387C2780007028 @default.
• W2912477387 hasConceptScore W2912477387C2780269544 @default.
• W2912477387 hasConceptScore W2912477387C2780559512 @default.
• W2912477387 hasConceptScore W2912477387C2780714102 @default.
• W2912477387 hasConceptScore W2912477387C2780942790 @default.
• W2912477387 hasConceptScore W2912477387C500558357 @default.
• W2912477387 hasConceptScore W2912477387C71924100 @default.
• W2912477387 hasIssue "3" @default.
• W2912477387 hasLocation W29124773871 @default.
• W2912477387 hasOpenAccess W2912477387 @default.
• W2912477387 hasPrimaryLocation W29124773871 @default.
• W2912477387 hasRelatedWork W1992861595 @default.
• W2912477387 hasRelatedWork W2001215986 @default.
• W2912477387 hasRelatedWork W2049397185 @default.
• W2912477387 hasRelatedWork W2080700961 @default.
• W2912477387 hasRelatedWork W2346584498 @default.
• W2912477387 hasRelatedWork W2356763381 @default.
• W2912477387 hasRelatedWork W2394376198 @default.
• W2912477387 hasRelatedWork W2399063111 @default.
• W2912477387 hasRelatedWork W2413550614 @default.
• W2912477387 hasRelatedWork W3196969625 @default.
• W2912477387 hasVolume "76" @default.
• W2912477387 isParatext "false" @default.
• W2912477387 isRetracted "false" @default.
• W2912477387 magId "2912477387" @default.
• W2912477387 workType "article" @default.