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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >Epigenetic regulation of fibrocyte differentiation?
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Epigenetic regulation of fibrocyte differentiation?

机译:纤维细胞分化的表观遗传调控?

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摘要

Production of extracellular proteins during non-adaptive fibrosis constitutes a major pathological feature that contributes to the physiologic abnormalities of cardiac hypertrophy and failure, as intersti-tially deposited collagen increases passive stiffness, induces adverse left ventricular remodeling, and propels diastolic dysfunction [1]. The development of cardiac fibrosis in the absence of cell death may have several origins and is often associated with inflammation [2,3]. Resident cardiac cells such as fibroblasts, endothelial, epithelial, or stem cells (mesenchymal and/or hematopoietic) may be activated by pro-inflammatory processes to differentiate into myofibroblasts, proliferate, and synthesize collagen that is secreted and deposited in the interstitial space [4,5]. In addition, several studies describe a critical role for the uptake and differentiation of primitive fibroblast precursor cells (i.e. fibrocyr.es) of bone marrow origin in pathological interstitial cardiac fibrosis [6-8].
机译:非适应性纤维化过程中细胞外蛋白质的产生构成了主要的病理特征,这是心肌肥大和衰竭的生理异常,因为间质沉积的胶原蛋白增加了被动僵硬,诱发了不良的左心室重构,并推动了舒张功能障碍[1]。在没有细胞死亡的情况下,心脏纤维化的发展可能有多个起源,并且通常与炎症有关[2,3]。驻留的心脏细胞,例如成纤维细胞,内皮细胞,上皮细胞或干细胞(间质和/或造血细胞)可以通过促炎过程激活,分化为肌成纤维细胞,增殖并合成分泌并沉积在间隙中的胶原蛋白[4]。 ,5]。此外,一些研究描述了在病理性间质性心肌纤维化中,骨髓来源的原始成纤维细胞前体细胞(即纤维性纤毛虫)的摄取和分化的关键作用[6-8]。

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