Forsythoside A Alleviates Hypertensive Nephropathy by Promoting Mitophagy and Inhibiting Ferroptosis via ASCL1-CCNB1/mTOR Pathway.
What this study shows
Forsythoside A binds ASCL1 and blocks the downstream CCNB1/mTOR axis, promoting mitophagy and suppressing ferroptosis to protect against Ang II-induced hypertensive nephropathy in mice — without lowering blood pressure.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: C57BL/6 mouse; NRK-52E rat kidney cells); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | C57BL/6 mouse; NRK-52E rat kidney cells |
| Journal | Journal of Ethnopharmacology |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/j.jep.2026.122346 · PMID 42665168 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Forsythoside A |
| Target | ASCL1-CCNB1/mTOR; mitophagy; ferroptosis |
| Model | Mouse; rat kidney epithelial cells |
| Effect | Reduced renal dysfunction markers and inflammation; increased mitophagy, decreased ferroptosis |
In the Atlas
Related topics
More studies on this topic
- Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule (2024)
- Urolithin A activates mitophagy via the AMPK-mTOR axis and modulates the gut-ceramide axis to ameliorate cardiac remodeling in HFpEF (2026)
Was this page useful?
Thank you. Your answer was counted anonymously.