Chronic Kidney Disease and Diabetes

This study shows that six months of physical inactivity in C57BL/6J mice on a high-fat diet does not cause chronic kidney disease but leads to early kidney injury markers.

This study shows Brg1 promotes fibroblast-myofibroblast transition in renal fibrosis and identifies Prune2 and PU.1 as downstream targets, with PFI-3 as a potential antifibrotic drug.

This study compares the antifibrotic effects of canagliflozin, irbesartan, and their combination in Dahl salt-sensitive rats on a high salt diet, showing improved renoprotection with combined therapy.

This study shows that EZH2 epigenetically suppresses PCK1, a gluconeogenic enzyme, promoting renal fibrosis, and that restoring PCK1 reduces fibrosis in CKD models.

This study uses multimodal single-cell sequencing to show that chromatin accessibility and genetic background influence diabetic kidney disease progression through cell-specific mechanisms.

The paper identifies p21 as a key mediator of hyperglycemic memory in diabetic kidney disease and shows that aPC signaling can reverse its effects.

This study shows that overexpressing DsbA-L in adipose tissue protects against diabetic kidney damage by reducing inflammation and improving kidney function through the adipo-renal axis.

This study shows emodin reduces renal interstitial fibrosis in rats by modulating the TIMP1/MM9 pathway.

This study identifies 16 genome-wide significant loci associated with diabetic kidney disease, including a protective variant in the COL4A3 gene.

This study uses EMRs and GWAS data to map CKD progression trajectories in African Americans with type 2 diabetes, identifying high-risk and low-risk pathways linked to APOL1 genotypes.