Mitochondrial Ferritin Overexpression Attenuates Ferroptosis and Mitochondrial Dysfunction by Reducing VDAC1 to Relieve MI/RI-Induced Damage.

ABSTRACT: Ischaemic cardiomyopathy is becoming one of the most prevalent cardiovascular diseases among the global elderly population. However, the underlying molecular mechanisms remain incompletely understood. Our previous study demonstrated that VDAC1 plays a significant role in MI/RI. Furthermore, FTMT plays a pivotal role in iron metabolism. However, the precise molecular functions of VDAC1 and FTMT in MI/RI remain to be elucidated. In vitro H9c2 cells A/R and in vivo SD rat MI/RI models were constructed. The present study reports that VDAC1 levels were increased and FTMT levels were decreased in A/R. The overexpression of VDAC1 resulted in an exacerbation of the A/R-induced injury, characterised by an increase in oxidative stress, a reduction in the GSH/GSSG ratio, the formation of reactive oxy

SUBMITTER: Yuan Y 

PROVIDER: S-EPMC12185369 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature