Pharmacological inhibition of apoptosis, necroptosis, and ferroptosis confers effective cardioprotection in post-myocardial infarction in rats.

ABSTRACT: Cardiovascular conditions account for millions of deaths globally. Myocardial infarction (MI) remains the foremost cause of cardiovascular death. Post-MI pathology can activate a diverse type of programmed cell death (PCD), which aggravates cardiac dysfunction and causes post-ischemic heart failure. Although various PCD inhibitors have shown potential efficacy against several cardiac complications, their roles in preventing or reducing myocardial loss and dysfunction in post-MI pathology have never been clarified. A rat model of MI was used in this study and post-MI rats were randomly assigned into 5 subgroups (n = 7/group): (1) vehicle (3%V/V DMSO), (2) enalapril (10 mg/kg), (3) zVAD-FMK (1 mg/kg), (4) Necrostatin-1 (1.65 mg/kg), or (5) Ferrostatin-1 (2 mg/kg). All treatments were given f

SUBMITTER: Piamsiri C 

PROVIDER: S-EPMC12375770 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature