Why the study?
Sex-specific mitochondrial alterations following chronic stress and ischemia-reperfusion injury are poorly characterized despite their implication in cardiac pathologies.
Does chronic restraint stress alter post-reperfusion cardiac mitochondrial function and redox balance in a sex-dependent manner in rats?
Does chronic restraint stress alter post-reperfusion cardiac mitochondrial function and redox balance in a sex-dependent manner in rats?
Chronic restraint stress induces sexually dimorphic alterations in cardiac mitochondrial function and oxidative stress following ischemia-reperfusion injury in a rat model.
Sex-specific mitochondrial resilience in stressed rat hearts cautions against uniform models; leaves open human translation and targeted therapies.
Although mitochondrial alterations are implicated in cardiac pathologies, sex-specific changes following chronic stress and ischemia-reperfusion injury are poorly characterized. Male and female Wistar rats underwent chronic restraint stress (CRS) for 4 weeks versus controls, whereafter ex vivo hearts were subjected to regional ischemia and reperfusion. Post-reperfusion hearts were dissected into ischemia-reperfused and non-ischemic regions with high-resolution mitochondrial respirometry, and oxidative stress assays performed. CRS males displayed increased routine and fatty acid β-oxidation respiration in non-ischemic tissues but lowered ETF-linked LEAK contributions to overall electron transfer system capacity ratios in ischemia-reperfused regions versus controls. CRS males exhibited lowered superoxide dismutase activity and increased lipid peroxidation in well-perfused regions versus controls. Female CRS hearts showed attenuated ETF-linked LEAK respiration and increased lipid peroxidation versus controls in non-ischemic tissue but a lowered RE ratio (measure of mitochondrial coupling) with ischemia-reperfusion. Our findings highlight the heart's sexually dimorphic response to chronic stress and ischemic injury, with female hearts showing oxidative damage in non-ischemic tissues together with relatively intact mitochondrial function in ischemia-reperfused tissues.
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Cairns et al. (2025) studied this question.
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