منابع مشابه
Macrophage-mediated cardiac fibrosis.
Both clinicians and investigators have long tended to consider cardiac fibrosis as a hopelessly unavoidable “final common pathway” of tissue injury. We are painfully familiar with the serious consequences of myocardial fibrosis, including diastolic dysfunction and promoting reentry dysrhythmias,1 but we seem to accept that diseased myocardium eventually develops fibrosis. However, only the most...
متن کاملInhibition of Toll-like receptor 2 reduces cardiac fibrosis by attenuating macrophage-mediated inflammation.
AIMS Toll-like receptor 2 (TLR2) is an important player in innate immunity, and recent studies have identified TLR2 as a critical mediator in cardiovascular diseases. Here, we investigated the involvement of TLR2 in angiotensin (Ang) II-induced cardiac fibrosis and the underlying mechanisms. METHODS AND RESULTS TLR2 knockout (TLR2 KO) mice (B6.129-Tlr2(tm1Kir)/) or wild-type (WT) mice (C57BL/...
متن کاملFunctional Relevance of Macrophage-mediated Inflammation to Cardiac Regeneration
Cardiovascular disease remains the leading cause of death worldwide and regenerative medicine is a promising therapeutic option for this disease. We have developed various techniques to attenuate the cardiac remodeling and to regenerate cardiovascular systems via stem cell application. Besides cell therapy, we are interested in the modulation of pathological inflammation mediated by macrophages...
متن کاملOxidative stress, fibrosis, and early afterdepolarization-mediated cardiac arrhythmias
Animal and clinical studies have demonstrated that oxidative stress, a common pathophysiological factor in cardiac disease, reduces repolarization reserve by enhancing the L-type calcium current, the late Na, and the Na-Ca exchanger, promoting early afterdepolarizations (EADs) that can initiate ventricular tachycardia and ventricular fibrillation (VT/VF) in structurally remodeled hearts. Increa...
متن کاملNorepinephrine Enhances Fibrosis Mediated by TGF- in Cardiac Fibroblasts
Cardiac fibrosis results from proliferation of interstitial fibroblasts and concomitant increased biosynthesis of extracellular matrix (ECM) components and is often complicated by cardiac hypertrophy. This study was conducted to investigate whether norepinephrine (NE) potentiates transforming growth factor(TGF)–induced cardiac fibrosis. The expression of the cardiac ECM proteins, plasminogen ac...
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ژورنال
عنوان ژورنال: Circulation Research
سال: 2004
ISSN: 0009-7330,1524-4571
DOI: 10.1161/01.res.0000143420.87587.9e