在纤维化、修复和再生过程中ECM的形成和降解。

Alejandro E Mayorca-Guiliani, Diana Julie Leeming, Kim Henriksen, Joachim Høg Mortensen, Signe Holm Nielsen, Quentin M Anstee, Arun J Sanyal, Morten A Karsdal, Detlef Schuppan
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引用次数: 0

摘要

反复损伤后不完善的器官修复尝试导致细胞外基质(ECM)的异常形成和组织结构的丧失。这种异常的ECM从细胞失调的结果变成持续纤维化细胞生态位的主干,损害有机功能并最终导致全身性疾病。在这里,我们回顾了我们目前对ECM结构的理解,器官特异性纤维化,消退,愈合和再生背后的机制,以及抗纤维化策略的发展。我们还讨论了生物标志物的设计,以研究纤维化病理生理,跟踪纤维化进展,全身损伤和纤维化消退。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ECM formation and degradation during fibrosis, repair, and regeneration.

Imperfect attempts at organ repair after repeated injury result in aberrant formation of extracellular matrix (ECM) and loss of tissue structure. This abnormal ECM goes from being a consequence of cellular dysregulation to become the backbone of a persistently fibrotic cell niche that compromises organic function and ultimately drives systemic disease. Here, we review our current understanding of the structure of the ECM, the mechanisms behind organ-specific fibrosis, resolution, healing and regeneration, as well as the development of anti-fibrotic strategies. We also discuss the design of biomarkers to investigate fibrosis pathophysiology, track fibrosis progression, systemic damage, and fibrosis resolution.

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