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SERCA Overexpression Improves Mitochondrial Quality Control and Attenuates Cardiac Microvascular Ischemia-Reperfusion

Ying Tan1, David Mui2, Sam Toan3

  • 1Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.

Molecular Therapy. Nucleic Acids
|November 24, 2020
PubMed

Insights

Sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) overexpression protects the heart from ischemia-reperfusion injury by improving cardiac microcirculation and mitochondrial function. This approach targets calcium, xanthine oxidase, and reactive oxygen species signaling pathways.

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Vascular Physiology

Background:

  • Myocardial ischemia-reperfusion (I/R) injury significantly impacts cardiac function, with coronary microcirculation often overlooked in protective strategies.
  • Understanding the molecular mechanisms of I/R injury in cardiac microvasculature is crucial for developing novel cardioprotective therapies.

Purpose of the Study:

  • To investigate the protective role of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) in cardiac microvascular endothelial cells (CMECs) against I/R injury.
  • To elucidate the mechanisms by which SERCA regulates mitochondrial quality control and protects against I/R-induced damage in the cardiac microcirculation.

Main Methods:

  • Gene delivery was used to overexpress SERCA in a model of cardiac microvascular I/R injury.
  • In vitro studies on CMECs assessed endothelial viability, barrier integrity, and cytoskeleton.
  • Mitochondrial quality control parameters (fusion, mitophagy, bioenergetics, biogenesis) were analyzed.
  • The role of calcium, xanthine oxidase (XO), and reactive oxygen species (ROS) signaling was examined.

Main Results:

  • SERCA overexpression attenuated lumen stenosis, microthrombus formation, and inflammation, while improving vascular relaxation.
  • In vitro, SERCA improved CMEC viability, barrier function, and cytoskeleton.
  • SERCA restored mitochondrial quality control disrupted by I/R injury.
  • Protective effects were linked to inhibition of calcium overload, XO, and ROS, with exogenous XO or calcium agonists abolishing these benefits.

Conclusions:

  • SERCA overexpression demonstrates significant cardioprotective effects against cardiac microvascular I/R injury.
  • SERCA preserves mitochondrial quality control by modulating calcium/XO/ROS signaling pathways.
  • Targeting SERCA offers a promising therapeutic strategy for mitigating myocardial I/R injury.

Keywords:
ROSSERCAXOcardiac microvascular I/R injurymitochondrial quality control

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