FOXC2 Alleviates Myocardial Ischemia-Reperfusion Injury in Rats through Regulating Nrf2/HO-1 Signaling Pathway

Rui Wang1, Yonggang Wu1, Shoutao Jiang1

  • 1Department of Cardiology, Guangzhou Hospital of Integrated Chinese and Western Medicine, Guangzhou, China.

Disease Markers
|December 3, 2021
PubMed
Abstract

Insights

Forkhead box C2 (FOXC2) protects against myocardial ischemia-reperfusion injury (MIRI) by reducing inflammation and oxidative stress. Upregulating FOXC2 promotes the Nrf2/HO-1 pathway, alleviating MIRI in rats.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Myocardial ischemia-reperfusion injury (MIRI) is a primary cause of mortality in cardiovascular disease.
  • Understanding the molecular mechanisms underlying MIRI is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role and mechanism of forkhead box C2 (FOXC2) in mitigating MIRI in a rat model.
  • To elucidate how FOXC2 influences oxidative stress and inflammation in the context of MIRI.

Main Methods:

  • Establishment of rat MIRI models via ischemia-reperfusion surgery.
  • Assessment of myocardial structure and function using TTC staining, echocardiography, LDH assay, and H&E staining.
  • Detection of FOXC2 expression changes and its effect on oxidative stress, inflammation, and the Nrf2/HO-1 pathway in vivo and in vitro (H9c2 cells).

Main Results:

  • FOXC2 expression was significantly reduced in MIRI rats compared to controls.
  • FOXC2 overexpression attenuated myocardial damage, reduced serum inflammatory factors, and enhanced antioxidant capacity (SOD1/2) in MIRI rats.
  • FOXC2 promoted the Nrf2/HO-1 signaling pathway, which was essential for its protective effects on myocardial cells.

Conclusions:

  • Reduced FOXC2 expression is associated with MIRI in rats.
  • FOXC2 exerts a protective effect against MIRI by suppressing inflammation and oxidative stress.
  • The protective mechanism involves the activation of the Nrf2/HO-1 signaling pathway by FOXC2.