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首页> 外文期刊>Circulation: An Official Journal of the American Heart Association >Interleukin-10 Inhibits Bone Marrow Fibroblast Progenitor Cell-Mediated Cardiac Fibrosis in Pressure-Overloaded Myocardium
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Interleukin-10 Inhibits Bone Marrow Fibroblast Progenitor Cell-Mediated Cardiac Fibrosis in Pressure-Overloaded Myocardium

机译:白细胞介素-10抑制骨髓成纤维细胞祖细胞介导的压力过载心肌中的心肌纤维化

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BACKGROUND: Activated fibroblasts (myofibroblasts) play a critical role in cardiac fibrosis; however, their origin in the diseased heart remains unclear, warranting further investigation. Recent studies suggest the contribution of bone marrow fibroblast progenitor cells (BM-FPCs) in pressure overload-induced cardiac fibrosis. We have previously shown that interleukin-10 (IL10) suppresses pressure overload-induced cardiac fibrosis; however, the role of IL10 in inhibition of BM-FPC-mediated cardiac fibrosis is not known. We hypothesized that IL10 inhibits pressure overload-induced homing of BM-FPCs to the heart and their transdifferentiation to myofibroblasts and thus attenuates cardiac fibrosis.
机译:背景:活性成纤维细胞(MyOfibroblasts)在心脏纤维化中发挥着关键作用; 然而,他们在患病的心脏中的起源仍然不清楚,需要进一步调查。 最近的研究表明骨髓成纤维细胞祖细胞(BM-FPC)在压力过载诱导的心纤纤膜中的贡献。 我们之前已经表明,白细胞介素-10(IL10)抑制压力过载引起的心肌纤维化; 然而,IL10在抑制BM-FPC介导的心肌纤维化中的作用是未知的。 我们假设IL10抑制BM-FPC的压力过载诱导的BM-FPC归巢,并将其转化为肌纤维细胞,从而衰减心脏纤维化。

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