Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs

作者：Gu, Yue-Yu; Liu, Xu-Sheng^*; Lan, Hui-Yao^*

来源：Molecular Therapy, 2024, 32(2): 313-324.

DOI：10.1016/j.ymthe.2023.12.009

• BETA-CELL PROLIFERATION
• DIABETIC KIDNEY INJURY
• TISSUE GROWTH-FACTOR
• TGF-BETA
• URETERAL OBSTRUCTION
• COLLAGEN EXPRESSION
• GENE-TRANSFER
• CONDITIONAL OVEREXPRESSION
• RADIATION NEPHROPATHY
• INTERSTITIAL FIBROSIS

Renal fibrosis is a characteristic hallmark of chronic kidney disease (CKD) that ultimately results in renal failure, leaving patients with few therapeutic options. TGF-b is a master regulator of renal fibrosis and mediates progressive renal fibrosis via both canonical and noncanonical signaling pathways. In the canonical Smad signaling, Smad3 is a key mediator in tissue fibrosis and mediates renal fibrosis via a number of noncoding RNAs (ncRNAs). In this regard, targeting Smad3-dependent ncRNAs may offer a specific therapy for renal fibrosis. This review highlights the significance and innovation of TGF-b/ Smad3-associated ncRNAs as biomarkers and therapeutic targets in renal fibrogenesis. In addition, the underlying mechanisms of these ncRNAs and their future perspectives in the treatment of renal fibrosis are discussed.

• 单位
  广州中医药大学; 南方医科大学; 广东省人民医院