ArticlePhysiological reports2025
An investigation into the sex dependence of post-reperfusion cardiac mitochondrial function and redox balance in chronically stressed rats.
Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- An investigation into the sex dependence of post-reperfusion cardiac mitochondrial function and redox balance in chronically stressed rats.Physiological reports · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
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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Registered trials
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