Kisspeptin-10 reduces cardiomyocyte injury in vitro via YY1/TFEB autophagy axis
In H9c2 cells after oxygen-glucose deprivation and reperfusion, 50 and 100 nM Kp-10 restored viability and autophagy markers; silencing YY1 or TFEB abolished the effect.
PR
By Priya Raman · Science Reporter
Oct 14 13:00 ETSource: Cytotechnology
The wire
- 01Cell-culture work found Kp-10 reversed reduced viability, raised MDA, and lowered SOD and CAT activity in OGD/R-stimulated H9c2 cardiomyocytes, with restored LC3-II/I, ATG5 and Beclin1.
- 02Kisspeptin is tracked on this beat for reproductive and sexual-health uses, so a cardiac autophagy mechanism broadens the questions around systemic exposure.
- 03The authors state validation in animal models is required before any clinical relevance can be assessed; this is an in-vitro model only.
From the source
Read at pubmed.ncbi.nlm.nih.govKisspeptin-10 alleviates OGD/R-induced H9c2 cardiomyocyte injury by triggering autophagy via regulating the YY1/TFEB axis
Cytotechnology · 2026 Dec · Li Q, Liu H, He Y et al.
Source URL https://pubmed.ncbi.nlm.nih.gov/42871171/
