IL-36与纤维化疾病的研究进展

Advances in study of IL-36 and fibrotic diseases

纤维化是由组织损伤触发的异常修复机制,伴随着细胞外基质(extracellular matrix, ECM)产生/降解的失衡以及在正常组织中的过度沉积,最终以器官功能障碍甚至衰竭而告终^([1])。纤维化几乎可见于所有慢性疾病的终末期阶段,死亡率在工业化国家中约占1/3以上,对人类健康构成严重威胁^([2-3])。然而,由于具体分子机制尚未明确,关于抗纤维化药物的开发仍在不断探索中。

Fibrosis is an abnormal repair process of the organism activated by tissue injury,with the typical pathological manifestation of excessive deposition of extracellular matrix,ultimately leading to the destruction of normal tis‐sue structure as well as organ hypofunction or even failure.The development of targeted anti-fibrotic drugs has been ham‐pered by the fact that the specific mechanism is not yet clear.There is growing evidence that interleukin-36(IL-36)has an important role in the development of fibrotic diseases.Aberrant expression of IL-36 cytokines is observed in idiopathic pulmonary fibrosis,liver fibrosis,renal interstitial fibrosis,inflammatory bowel disease-associated intestinal fibrosis,and cardiac fibrosis.Inhibition or knockdown of IL-36 can effectively prevent or even reverse fibrotic lesions,and its mecha‐nism is closely related to the regulation of immune cell responses,the activation of fibroblasts,and the regulation of related enzyme activity.In this paper,we review the recent research progress of IL-36 and its expression and pro-fibrotic mecha‐nisms in different fibrotic diseases in order to provide a reference for further research.