Potential Therapeutic Targets for Cardiac Fibrosis
نویسندگان
چکیده
منابع مشابه
Potential therapeutic targets for cardiac fibrosis: TGFbeta, angiotensin, endothelin, CCN2, and PDGF, partners in fibroblast activation.
Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because of a persistent tissue repair program. During connective tissue repair, "activated" fibroblasts migrate into the wound area, where they synthesize and remodel newly created extracellular matrix. The specialized type of fibroblast responsible for this action is the alpha-smooth muscle...
متن کاملPotential Therapeutic Targets for Cardiac Fibrosis TGF , Angiotensin, Endothelin, CCN2, and PDGF, Partners in Fibroblast Activation
Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because of a persistent tissue repair program. During connective tissue repair, “activated” fibroblasts migrate into the wound area, where they synthesize and remodel newly created extracellular matrix. The specialized type of fibroblast responsible for this action is the -smooth muscle acti...
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Cardiac fibrosis, in response to injury and stress, is central to a broad constellation of cardiovascular diseases. Fibrosis decreases myocardial wall compliance due to extracellular matrix (ECM) accumulation, leading to impaired systolic and diastolic function and causing arrhythmogenesis. Although some conventional drugs, such as β-blockers and renin-angiotensin-aldosterone system (RAAS) inhi...
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Inflammatory and fibrotic responses to myocardial damage are essential for cardiac repair; however, these responses often result in extensive fibrotic remodeling with impaired systolic function. Recent reports have suggested that such acute phase responses provide a favorable environment for endogenous cardiac regeneration, which is mainly driven by the division of pre-existing cardiomyocytes (...
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This commentary highlights the findings by Tao et al. (Theranostics 2016; 6: 2068-2083) that targeting miR-433 may be a potential therapeutic strategy for myocardial fibrosis and subsequently discusses the obstacles and prospects associated with the application of therapeutic microRNAs in anti-fibrosis treatment.
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ژورنال
عنوان ژورنال: Circulation Research
سال: 2010
ISSN: 0009-7330,1524-4571
DOI: 10.1161/circresaha.110.217737