NR4A1 promotes oxidative stresses after myocardial ischemia reperfusion injury in aged mice

Myocardial infarction (MI) is a serious disease which is responsible for major death in the elderly. Myocardial oxidative stress contributes to pathophysiology of MI. The nuclear receptor subfamily 4 group A member 1 (NR4A1) has been shown to regulate oxidative stress in several diseases. However, the precise roles of NR4A1 in MI-induced oxidative stress in elderly remain unknown. In present study, the effects of NR4A1 deficiency on oxidative stress were evaluated in aged MI mice. A MI aged mice model was established in wide-type (WT) and NR4A1 deficient mice. The expression of NR4A1, oxidative stress markers was measured. The myocardial functions were monitored. NR4A1 was upregulated in aged MI WT mice, which was positively correlated to the elevated oxidative stress. NR4A1 deficient MI mice had significantly decreased expression of oxidative stress markers malondialdehyde and hydrogen peroxide while had improved myocardial function. In summary, NR4A1 deficiency could attenuate oxidative stress in aged MI mice.

Automated summary

NR4A1 deficiency can attenuate oxidative stress in aged MI mice and improve myocardial function.