ACSL4 contributes to ferroptosis-mediated rhabdomyolysis in exertional heat stroke.

ABSTRACT:

Background

Rhabdomyolysis (RM) is a common complication of exertional heat stroke (EHS) and constitutes a direct cause of death. However, the mechanism underlying RM following EHS remains unclear.

Methods

The murine EHS model was prepared by our previous protocol. RNA sequencing is applied to identify the pathological pathways that contribute to RM following EHS. Inhibition of the acyl-CoA synthetase long-chain family member 4 (ACSL4) was achieved by RNA silencing in vitro prior to ionomycin plus heat stress exposure or pharmacological inhibitors in vivo prior to heat and exertion exposure. The histological changes, the iron accumulation, oxidized phosphatidylethanolamines species, as well as histological evaluation and levels of lipid metabolites in skeletal muscle tissues

SUBMITTER: He S 

PROVIDER: S-EPMC9178366 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature