ArticleFrontiers in cardiovascular medicine2026
Plasma ALKBH5 depletion during severe intermittent hypoxia and its attenuation by galectin-3 inhibition: an experimental rat study.
Article in Frontiers in cardiovascular medicine, 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
Background: Intermittent hypoxia (IH), the pathophysiological hallmark of obstructive sleep apnea (OSA), promotes oxidative stress and cardiovascular remodeling. Galectin-3 (Gal-3) is a key mediator of hypoxia-associated inflammatory cardiac injury. ALKBH5, an m6A RNA demethylase detectable in plasma, has not been systematically characterized during hypoxic cardiovascular stress. This experimental study examined plasma ALKBH5 responses to graded IH and evaluated whether pharmacologic Gal-3 inhibition with modified citrus pectin (MCP) modulates circulating ALKBH5 levels and associated cardiac histopathology. Methods: Male Sprague-Dawley rats ( Results: Plasma Gal-3 increased in a severity-dependent manner with IH (Control: 18.4 ± 3.2; MIH: 34.7 ± 5.8; SIH: 48.2 ± 7.1 ng/mL; Conclusion: Severe intermittent hypoxia has been linked to a drop in circulating ALKBH5 levels, whereas pharmacological inhibition of galectin-3 has been associated with maintaining plasma ALKBH5 concentrations and a significant reduction of hypoxia-induced myocardial pathological damage in an experimental rat model. These findings suggest circulating ALKBH5 as a hypoxia-responsive molecular signal controlled by inflammatory pathways; however, more mechanistic and longitudinal investigations are necessary to characterize its biological significance and possible translational value.
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