Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", Piazza Giulio Cesare 1, I-70124 Bari, Italy.
Int J Mol Sci. 2023 May 21;24(10):9060. doi: 10.3390/ijms24109060.
Autoimmunity is a chronic process resulting in inflammation, tissue damage, and subsequent tissue remodelling and organ fibrosis. In contrast to acute inflammatory reactions, pathogenic fibrosis typically results from the chronic inflammatory reactions characterizing autoimmune diseases. Despite having obvious aetiological and clinical outcome distinctions, most chronic autoimmune fibrotic disorders have in common a persistent and sustained production of growth factors, proteolytic enzymes, angiogenic factors, and fibrogenic cytokines, which together stimulate the deposition of connective tissue elements or epithelial to mesenchymal transformation (EMT) that progressively remodels and destroys normal tissue architecture leading to organ failure. Despite its enormous impact on human health, there are currently no approved treatments that directly target the molecular mechanisms of fibrosis. The primary goal of this review is to discuss the most recent identified mechanisms of chronic autoimmune diseases characterized by a fibrotic evolution with the aim to identify possible common and unique mechanisms of fibrogenesis that might be exploited in the development of effective antifibrotic therapies.
自身免疫是一种慢性过程，导致炎症、组织损伤，随后发生组织重塑和器官纤维化。与急性炎症反应不同，致病纤维化通常是由自身免疫性疾病的慢性炎症反应引起的。尽管具有明显的病因和临床结局差异，但大多数慢性自身免疫性纤维性疾病的共同点是持续和持续产生生长因子、蛋白水解酶、血管生成因子和纤维生成细胞因子，这些因子共同刺激结缔组织成分的沉积或上皮到间充质转化（EMT），逐渐重塑和破坏正常组织结构，导致器官衰竭。尽管它对人类健康有巨大影响，但目前尚无批准的治疗方法可直接针对纤维化的分子机制。本综述的主要目的是讨论最近发现的以纤维化演变为特征的慢性自身免疫性疾病的机制，旨在确定可能在开发有效抗纤维化治疗方法中利用的纤维发生的共同和独特机制。
