ArticleCellular and molecular life sciences : CMLS2026
Chronic hypoxia protects the mouse heart from oxidative stress via HIF-1α-mitochondria crosstalk.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Oxidative stress in bladder outlet obstruction: a narrative review.Translational andrology and urology · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
Adaptation to chronic hypoxia (CH) enhances myocardial tolerance to ischemia/reperfusion injury and is closely associated with stabilization of hypoxia-inducible factor-1 alpha (HIF-1α), a central transcription factor in hypoxic response. Given the central role of mitochondria in cardiac pathophysiology, we investigated the contribution of HIF-1α to cellular mechanisms underlying CH-induced cardioprotection, with a focus on proteomic remodeling, antioxidant defense, and regulation of the mitochondrial permeability transition pore (mPTP). Adult male wild-type and heterozygous Hif1a knockout mice were exposed to intermittent CH (7000 m, 8 h/day, 4 weeks) or kept under normoxia. Isolated perfused hearts treated with cyclosporine A, an inhibitor of mPTP opening, were subjected to global ischemia/reperfusion insult for infarct size determination. Quantitative label-free proteomics was conducted to assess HIF-1α-dependent changes. We evaluated oxidative stress, measured levels of proteins associated with antioxidant defense and mPTP regulation. In parallel, a proof-of-concept study was performed in transfected AC16 cardiomyocytes exposed to H
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