Yamashita Noriyuki, Kramann Rafael
Department of Nephrology and Clinical Immunology, RWTH Aachen University, Aachen, Germany; Department of Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Department of Nephrology and Clinical Immunology, RWTH Aachen University, Aachen, Germany; Department of Internal Medicine, Nephrology, and Transplantation, Erasmus Medical Center, Rotterdam, The Netherlands.
Trends Endocrinol Metab. 2024 Jan;35(1):31-48. doi: 10.1016/j.tem.2023.09.001. Epub 2023 Sep 28.
Kidney fibrosis is the final common pathway of virtually all chronic kidney diseases (CKDs) and is therefore considered to be a promising therapeutic target for these conditions. However, despite great progress in recent years, no targeted antifibrotic therapies for the kidney have been approved, likely because the complex mechanisms that initiate and drive fibrosis are not yet completely understood. Recent single-cell genomic approaches have allowed novel insights into kidney fibrosis mechanisms in mouse and human, particularly the heterogeneity and differentiation processes of myofibroblasts, the role of injured epithelial cells and immune cells, and their crosstalk mechanisms. In this review we summarize the key mechanisms that drive kidney fibrosis, including recent advances in understanding the mechanisms, as well as potential routes for developing novel targeted antifibrotic therapeutics.
肾纤维化是几乎所有慢性肾脏病（CKD）的最终共同通路，因此被认为是这些疾病颇具前景的治疗靶点。然而，尽管近年来取得了巨大进展，但尚无针对肾脏的抗纤维化靶向疗法获批，这可能是因为启动和驱动纤维化的复杂机制尚未完全明确。最近的单细胞基因组学方法使我们对小鼠和人类肾纤维化机制有了新的认识，特别是肌成纤维细胞的异质性和分化过程、受损上皮细胞和免疫细胞的作用及其相互作用机制。在本综述中，我们总结了驱动肾纤维化的关键机制，包括在理解这些机制方面的最新进展，以及开发新型抗纤维化靶向疗法的潜在途径。
