ArticleFrontiers in physiology2026
Integrated proteomics and metabolomics reveal mechanisms of blood pressure reduction in spontaneously hypertensive rats under hypoxic conditions.
Article in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: High-altitude hypoxic environments markedly affect the cardiovascular system and blood pressure regulation. However, the molecular mechanisms underlying decreases in blood pressure induced by chronic hypoxia exposure in spontaneously hypertensive rats (SHRs) remain unclear. Therefore, we systematically elucidated the mechanisms by which chronic high-altitude hypoxia exposure induces adaptive molecular remodeling and subsequent decreases in blood pressure SHRs. Methods: SHRs were randomly divided into control (SHR-C, 1660 m; PaO Results and discussion: The SHR-H group exhibited pronounced reductions in systolic blood pressure, diastolic blood pressure, and mean arterial pressure compared with the SHR-C group. Proteomics analysis identified 185 differentially expressed proteins (161 upregulated and 24 downregulated). According to functional enrichment analysis, the upregulated proteins were considerably enriched in energy metabolism pathways, whereas downregulated proteins were associated with inflammatory and stress responses. Integrated protein-metabolite network analysis revealed that the tricarboxylic acid cycle was the central hub, and western blotting validated the upregulation of mitochondrial-associated proteins. Metabolomics confirmed energy metabolism reprogramming by detecting markers of enhanced fatty acid oxidation. Overall, this study provides correlative mechanistic insights into the cardiovascular effects of high-altitude hypoxic environments and proposes novel metabolic intervention strategies for hypertension, though direct functional validation is necessary to confirm the proposed mechanisms.
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