Authors
Xiyue Tian, Rangyue Han, Xiaojiao Gu, Yuqing Li, Honglian Wang, Qiongdan Hu, Li Wang
Published in
Clinical nephrology. Aug 10, 2026. Epub Aug 10, 2026.
Abstract
Podocyte injury is a pivotal driver of chronic kidney disease (CKD) progression in focal segmental glomerulosclerosis (FSGS). Although hederagenin (HDG) has shown promise in the treatment of CKD, its specific protective effects against podocyte injury in FSGS, along with its underlying pharmacological mechanisms, remain to be fully elucidated.
Potential protein targets of HDG and FSGS-related genes were retrieved from the Genecards database. Molecular docking was performed to validate binding interactions between HDG and key targets. Building on findings from adriamycin (ADR)-induced FSGS mouse and MPC5 cell line studies, HDG's inhibitory effect on podocyte injury in FSGS was further confirmed.
A total of 103 potential HDG targets and 2378 FSGS-related targets were identified. Integrated drug-disease network and protein-protein interaction (PPI) analyses suggested potential mechanisms for HDG in FSGS treatment. Molecular docking pinpointed IL-6 and NOS2 as therapeutic targets, indicating their involvement in HDG's inhibitory effects. In vivo and in vitro experiments demonstrated that HDG alleviated renal injury in ADR-induced FSGS in mice and attenuated TGF-β1-induced damage in MPC5 cells. Furthermore, HDG significantly reduced both mRNA and protein expression levels of IL-6 and NOS2.
HDG protects podocytes from injury by inhibiting IL-6 and NOS2 in FSGS, which is consistent with the results predicted by network pharmacological analysis. These findings support HDG as a promising therapeutic candidate for FSGS treatment.
PMID:
42572870
Bibliographic data and abstract were imported from PubMed on 10 Aug 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 6
- Comments 0