Jia X. Zhang
Nanjing, China
Last Updated: 09/26/2026
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Found 8 publications
Deficiency of Growth Arrest and DNA Damage-Inducible 45 α -R-Loop Pathway and Kidney Injury in Diabetic Nephropathy.
Journal: Journal of the American Society of Nephrology : JASN
Published: October 09, 2024
Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease.
Journal: Cell death and differentiation
Published: February 10, 2024
Outer membrane vesicles derived from gut microbiota mediate tubulointerstitial inflammation: a potential new mechanism for diabetic kidney disease.
Journal: Theranostics
Published: March 25, 2023
Activation of acetyl-CoA synthetase 2 mediates kidney injury in diabetic nephropathy.
Journal: JCI insight
Published: October 06, 2022
GPR43 activation-mediated lipotoxicity contributes to podocyte injury in diabetic nephropathy by modulating the ERK/EGR1 pathway.
Journal: International journal of biological sciences
Published: July 07, 2021
Deposition of platelet-derived microparticles in podocytes contributes to diabetic nephropathy.
Journal: International urology and nephrology
Published: May 21, 2021
GPR43 deficiency protects against podocyte insulin resistance in diabetic nephropathy through the restoration of AMPKα activity.
Journal: Theranostics
Published: November 30, 2020
Dysbiosis of intestinal microbiota mediates tubulointerstitial injury in diabetic nephropathy via the disruption of cholesterol homeostasis.
Journal: Theranostics
Published: September 23, 2019
Showing 1-8 of 8
Last Updated: 09/26/2026