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• W2061511179 endingPage "280" @default.
• W2061511179 startingPage "268" @default.
• W2061511179 abstract "Tissue inhibitor of metalloproteinases (TIMPs) can mediate myocardial remodelling, hypertrophy, and fibrosis in heart disease. We investigated the impact of TIMP2 vs. TIMP3 deficiency in angiotensin II (Ang II)-induced myocardial remodelling and cardiac dysfunction.TIMP2(-/-), TIMP3(-/-), and wild-type (WT) mice received Ang II/saline (Alzet pump) for 2 weeks. Ang II infusion resulted in enhanced myocardial hypertrophy and lack of fibrosis in TIMP2(-/-), and conversely, excess fibrosis without hypertrophy in TIMP3(-/-) mice. Echocardiographic imaging revealed preserved ejection fraction in all groups; however, exacerbated left ventricular (LV) diastolic dysfunction was detected in Ang II-infused TIMP2(-/-) and TIMP3(-/-) mice, despite the suppressed Ang II-induced hypertension in TIMP3(-/-) mice. Enhanced hypertrophy in TIMP2(-/-) mice impaired active relaxation, while excess fibrosis in TIMP3(-/-) mice increased LV passive stiffness. Adult WT cardiomyocytes, only when co-cultured with cardiac fibroblasts, exhibited Ang II-induced hypertrophy which was suppressed in TIMP3(-/-) cardiomyocytes. In vitro studies on adult cardiofibroblasts (quiescent and cyclically stretched), and in vivo analyses, revealed that the increased fibrosis in TIMP3(-/-)-Ang II hearts is due to post-translational stabilization and deposition of collagen by matricellular proteins [osteopontin and Secreted Protein Acidic and Rich in Cysteine (SPARC)], which correlated with increased inflammation, rather than increased de novo synthesis. Reduced cross-linking enzymes, LOX and PLOD1, could underlie suppressed collagen deposition in TIMP2(-/-)-Ang II hearts.TIMP2 and TIMP3 play fundamental and differential roles in mediating pathological remodelling, independent from their MMP-inhibitory function. TIMP2(-/-) and TIMP3(-/-) mice provide a unique opportunity to study myocardial hypertrophy and fibrosis independently, and their impact on cardiac dysfunction." @default.
• W2061511179 created "2016-06-24" @default.
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• W2061511179 date "2014-04-01" @default.
• W2061511179 modified "2023-10-13" @default.
• W2061511179 title "Differential role of TIMP2 and TIMP3 in cardiac hypertrophy, fibrosis, and diastolic dysfunction" @default.
• W2061511179 cites W1547783254 @default.
• W2061511179 cites W164205712 @default.
• W2061511179 cites W1970490335 @default.
• W2061511179 cites W1975977239 @default.
• W2061511179 cites W1981421887 @default.
• W2061511179 cites W1985850316 @default.
• W2061511179 cites W1986610146 @default.
• W2061511179 cites W1987929268 @default.
• W2061511179 cites W1997961928 @default.
• W2061511179 cites W2002132236 @default.
• W2061511179 cites W2004247840 @default.
• W2061511179 cites W2004540849 @default.
• W2061511179 cites W2005868264 @default.
• W2061511179 cites W2008587727 @default.
• W2061511179 cites W2009075375 @default.
• W2061511179 cites W2014639995 @default.
• W2061511179 cites W2017049923 @default.
• W2061511179 cites W2020087937 @default.
• W2061511179 cites W2020803682 @default.
• W2061511179 cites W2021275308 @default.
• W2061511179 cites W2029269323 @default.
• W2061511179 cites W2034264001 @default.
• W2061511179 cites W2041050431 @default.
• W2061511179 cites W2041966195 @default.
• W2061511179 cites W2042800560 @default.
• W2061511179 cites W2044427990 @default.
• W2061511179 cites W2045142779 @default.
• W2061511179 cites W2046275929 @default.
• W2061511179 cites W2050561023 @default.
• W2061511179 cites W2057490727 @default.
• W2061511179 cites W2060072724 @default.
• W2061511179 cites W2067385119 @default.
• W2061511179 cites W2067406160 @default.
• W2061511179 cites W2068569386 @default.
• W2061511179 cites W2072085629 @default.
• W2061511179 cites W2076812384 @default.
• W2061511179 cites W2087173527 @default.
• W2061511179 cites W2088184271 @default.
• W2061511179 cites W2089530876 @default.
• W2061511179 cites W2097707959 @default.
• W2061511179 cites W2100592123 @default.
• W2061511179 cites W2100629191 @default.
• W2061511179 cites W2102308209 @default.
• W2061511179 cites W2102489984 @default.
• W2061511179 cites W2107726585 @default.
• W2061511179 cites W2109281287 @default.
• W2061511179 cites W2109967971 @default.
• W2061511179 cites W2111290043 @default.
• W2061511179 cites W2112613176 @default.
• W2061511179 cites W2117025765 @default.
• W2061511179 cites W2119871412 @default.
• W2061511179 cites W2121891227 @default.
• W2061511179 cites W2127039247 @default.
• W2061511179 cites W2128374399 @default.
• W2061511179 cites W2130674647 @default.
• W2061511179 cites W2130895647 @default.
• W2061511179 cites W2130995100 @default.
• W2061511179 cites W2132250523 @default.
• W2061511179 cites W2134213199 @default.
• W2061511179 cites W2134948873 @default.
• W2061511179 cites W2135888652 @default.
• W2061511179 cites W2137784332 @default.
• W2061511179 cites W2138738317 @default.
• W2061511179 cites W2139068414 @default.
• W2061511179 cites W2142285130 @default.
• W2061511179 cites W2143836365 @default.
• W2061511179 cites W2148080571 @default.
• W2061511179 cites W2149718877 @default.
• W2061511179 cites W2149841172 @default.
• W2061511179 cites W2153195779 @default.
• W2061511179 cites W2154009047 @default.
• W2061511179 cites W2161321429 @default.
• W2061511179 cites W2161923979 @default.
• W2061511179 cites W2164972289 @default.
• W2061511179 cites W2168850679 @default.
• W2061511179 cites W2169304578 @default.
• W2061511179 cites W2546760584 @default.
• W2061511179 doi "https://doi.org/10.1093/cvr/cvu072" @default.
• W2061511179 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24692173" @default.
• W2061511179 hasPublicationYear "2014" @default.
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