Deletion of Smad3 prevents renal fibrosis and inflammation in type 2 diabetic nephropathy

• Published in: Metabolism, clinical and experimental Vol. 103; p. 154013
• Main Authors: Xu, Bi-Hua, Sheng, Jingyi, You, Yong-Ke, Huang, Xiao-Ru, Ma, Ronald C.W., Wang, Qingwen, Lan, Hui-Yao
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.02.2020
• Subjects: Albuminuria - complications; Albuminuria - genetics; Animals; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - genetics; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - genetics; Diabetic Nephropathies - genetics; Diabetic Nephropathies - prevention & control; Diabetic nephropathy; Female; Fibrosis; Fibrosis - genetics; Fibrosis - prevention & control; Gene Deletion; Inflammation; Kidney - pathology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Smad3 and TGF-β; Smad3 Protein - genetics; EndoMT; T1DN; MCP-1; PAS; IHC; JNK; LncRNA; DN; ICAM-1; T2DN; CTGF; SE; GBM; ANOVA; Col-IV; STZ; P-NF-κB/65; TGF-β; Diabetic nephropathy; AngII; WT; AGE; DAB; KO; VEGF; Inflammation; IL-8; MAPK; EMT; IL-6; PASM; UUO; ACR; P-IκBα; SIS3; Smad3 and TGF-β; TNF-α; Fibrosis; Col-I; P-Smad3; PCR; Erk

Transforming growth factor (TGF)-β/Smad3 signaling is highly activated in kidneys of patients with type 2 diabetic nephropathy (T2DN), however, the precise role of Smad3 in the pathogenesis of diabetic nephropathy remains unclear. Smad3 knockout (KO)-db/db mice were generated by intercrossing of mal...