Protective effect of compound K against podocyte injury in chronic kidney disease by maintaining mitochondrial homeostasis.

ABSTRACT: Chronic kidney disease (CKD) stands as a formidable global health challenge, often advancing to end-stage renal disease (ESRD) with devastating morbidity and mortality. At the central of this progression lies podocyte injury, a critical determinant of glomerular dysfunction. Compound K (CK), a bioactive metabolite derived from ginsenoside, has emerged as a compelling candidate for nephroprotective therapy. Here, we unveil the profound therapeutic potential of CK in a folic acid (FA)-induced CKD mouse model, demonstrating its ability to restore renal function and mitigate podocyte injury. CK exerted its nephroprotective effects by reinforcing inter-podocyte junctions, suppressing aberrant podocyte motility, and preventing podocyte detachment and apoptosis, thereby safeguarding the glomerula

SUBMITTER: Huang F 

PROVIDER: S-EPMC11696807 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature