Issue Archive

Transforming growth factor-β and renal fibrosis

MENG Xiao-Ming¹, LAN Hui-Yao^2,*

¹School of Pharmacy, Anhui Medical University; Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education; The Key Laboratory of Major Autoimmune Diseases, Hefei 230032, China；²Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China; Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen 518172, China

Abstract

Transforming growth factor-β (TGF-β) is a driving force of renal fibrosis, which may lead to chronic kidney diseases and even end stage renal diseases. By activating canonical and non-canonical signaling pathways, TGF-β promotes the synthesis of extracellular matrix while preventing their degradation. In the injured kidney, TGF-β induces apoptosis, proliferation and fibrotic response of renal cells including epithelial cells, endothelial cells, podocytes, fibroblasts, pericytes and macrophages, and it also promotes transdifferentiation, activation and proliferation of myofibroblasts. Additionally, TGF-β exerts profibrotic effects by interplaying with other signaling pathways like BMP-7, Wnt/β-catenin and MAP kinase. Smad3 is the central pathological gene in renal fibrosis, and epigenetic regulation of TGF-β/Smad3 is a hot topic in kidney field. Although direct targeting TGF-β may cause side effects including tumorigenesis and immune diseases, the therapeutic strategies targeting the balance of downstream Smad3 and Smad7 may prevent or delay the progression of fibrotic kidney disease.

Key words: renal fibrosis; TGF-β/Smads; epigenetic modifications; myofibroblast; Macrophage

Received: 2018-06-05　　Accepted: 2018-09-21

Corresponding author: 蓝辉耀　　E-mail: hylan@cuhk.edu.hk

DOI: 10.13294/j.aps.2018.0085

Citing This Article：

MENG Xiao-Ming, LAN Hui-Yao. Transforming growth factor-β and renal fibrosis. Acta Physiol Sin 2018; 70 (6): 612-622 (in Chinese with English abstract).