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纤维化（fibrosis）是以器官组织内纤维结缔组织异常增多、实质细胞减少为特征的病理改变，多由损伤修复过程中纤维结缔组织过度增生引起，可导致器官结构破坏和功能减退。 Fibrosis can be a normal connective tissue deposition or excessive tissue deposition caused by a disease. 纤维化 （英語： fibrosis）是指正常 器官 或 组织 因受到超出自身 修复能力 的损伤后，受损处转化为由 成纤维细胞 与含有 胶原蛋白 、 纤连蛋白 的 细胞外基质 构成的纤维化组织的过程 [1][2] 。
近日，来自美国辉瑞公司全球研究中心的 Thomas A. Wynn 团队在 Nature 杂志上发表了一篇题为 Fibrosis: from mechanisms to medicines 的综述，在这篇文章中，作者详 细阐述了纤维化关键分子机制的最新研究进展，并讨论了如何将这些信息转化为抗纤维化治疗的开发策略。 Fibrosis, also known as fibrotic scarring, is the development of fibrous connective tissue in response to an injury Therapeutic translation for fibrotic disease
Cellular and molecular mechanisms of fibrosis
The master regulator of fibrosis Large white spots caused a strong focal fibrosis and atrophy of lobules, that disappeared completely in the centre. 成纤维细胞是一类组织内特殊间质细胞，在纤维化疾病的发病机制中发挥核心作用。纤维化疾病可累及多个重要器官系统，在全球范围内导致严重的. Abstract fibrosis is a pathophysiological mechanism involved in chronic and progressive diseases that results in excessive tissue scarring.
Some important signaling pathways associated with fibrosis are also introduced.
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