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- W2072749062 abstract "This editorial refers to ‘Differential role of TIMP2 and TIMP3 in cardiac hypertrophy, fibrosis, and diastolic dysfunction’ by D. Fan et al. , pp. 268–280, this issue. Heart failure with preserved ejection fraction (HFPEF) is a major cause of morbidity and mortality and constitutes a significant portion of medical care costs. Being as deadly as systolic HF, it completely lacks effective therapy beside the management of its metabolic risk factors including diabetes, obesity and hyperlipidaemia, and hypertension. Typical medication that helps systolic HF (HF with reduced EF, HFREF) patients, such as beta-blockade and angiotensin-converting enzyme inhibitors, are not successful in HFPEF patients.1HFPEF is characterized by cardiomyocyte hypertrophy and increased interstitial fibrosis, both leading to enhanced cardiac stiffness and dysfunction.2 Therapeutic strategies targeting the fundamental underpinnings of hypertrophy and fibrosis remain an unmet medical need and hence represent an important area for research and development.The present paper by Fan et al. 3 reveals paradoxical roles for tissue inhibitors of MMPs (TIMP)-2 and TIMP3 in Angiotensin-II (AngII)-induced cardiac fibrosis. Whereas the absence of TIMP2 enhanced hypertrophy without affecting fibrosis, lacking TIMP3 increased cardiac fibrosis along with enhanced cardiac inflammation. These findings first of all underline the anti-inflammatory and parallel anti-fibrotic properties of TIMP3, also observed in other organs. Its absence enhanced immune activation and fibrosis in mouse models of bleomycine-induced pulmonary disease,4 nephritis,5 and auto-immune hepatitis.6Matrix metalloproteinases (MMPs) and their …" @default.
- W2072749062 created "2016-06-24" @default.
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- W2072749062 date "2014-06-22" @default.
- W2072749062 modified "2023-09-25" @default.
- W2072749062 title "Fibrosis or hypertrophy: let TIMPs decide" @default.
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- W2072749062 doi "https://doi.org/10.1093/cvr/cvu160" @default.
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