MicroRNA-668 alleviates renal fibrosis through PPARα/PGC-1α pathway DOI Creative Commons
Xinran Wang,

Zhoupeng Gu,

Yan Huang

et al.

European journal of medical research, Journal Year: 2024, Volume and Issue: 29(1)

Published: Dec. 28, 2024

The involvement of microRNA-668 (miR-668) in the onset and progression renal fibrosis remains unclear. To this end, we aimed to explore relevant mechanism miR-668 fibrosis. C57BL/6 J male mice were randomly divided into sham-operated, unilateral ureteral obstruction (UUO), UUO-fenofibrate groups. Based on transfection drug intervention, HK-2 cells blank control, TGF-β1, TGF-β1 + fenofibrate (PPARα agonist), mimics-NC, miR-668, mimics-NC fenofibrate, GW6471 inhibitor), pathological changes tissues observed by hematoxylin–eosin (HE) Masson staining. expression PPARα, PGC-1α, E-cadherin, Collagen III (Col III), α-SMA or was detected western blot, immunohistochemical analyses real-time quantitative polymerase chain reaction. regulatory effect PPARα verified dual-luciferase reporter assay. PGC-1α decreased UUO TGF-β1-induced cells, which improved fenofibrate. Compared non-transfected group, TGF-β1-stimulated increased Col miR-668-transfected group. assay indicated hsa-mir-668-3p PPARα. MiR-668 can target positively regulate PPARα/PGC-1α pathway alleviate

Language: Английский

Cardioprotective Effects of the Jiming Formula on Myocardial Metabolism in Mice with Myocardial Infarction via the AMPK/SIRT1/PGC-1α Pathway DOI
Xinyi Fan,

Xiaoqi Wei,

Wendi Wang

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156727 - 156727

Published: April 1, 2025

Language: Английский

Citations

0
MicroRNA-668 alleviates renal fibrosis through PPARα/PGC-1α pathway DOI Creative Commons
Xinran Wang,

Zhoupeng Gu,

Yan Huang

et al.

European journal of medical research, Journal Year: 2024, Volume and Issue: 29(1)

Published: Dec. 28, 2024

The involvement of microRNA-668 (miR-668) in the onset and progression renal fibrosis remains unclear. To this end, we aimed to explore relevant mechanism miR-668 fibrosis. C57BL/6 J male mice were randomly divided into sham-operated, unilateral ureteral obstruction (UUO), UUO-fenofibrate groups. Based on transfection drug intervention, HK-2 cells blank control, TGF-β1, TGF-β1 + fenofibrate (PPARα agonist), mimics-NC, miR-668, mimics-NC fenofibrate, GW6471 inhibitor), pathological changes tissues observed by hematoxylin–eosin (HE) Masson staining. expression PPARα, PGC-1α, E-cadherin, Collagen III (Col III), α-SMA or was detected western blot, immunohistochemical analyses real-time quantitative polymerase chain reaction. regulatory effect PPARα verified dual-luciferase reporter assay. PGC-1α decreased UUO TGF-β1-induced cells, which improved fenofibrate. Compared non-transfected group, TGF-β1-stimulated increased Col miR-668-transfected group. assay indicated hsa-mir-668-3p PPARα. MiR-668 can target positively regulate PPARα/PGC-1α pathway alleviate

Language: Английский

Citations

0