水素による慢性間欠的低酸素誘発血管内皮細胞老化の軽減：ミトコンドリアオートファジーと酸化ストレス制御を介したメカニズム解析
Chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnea (OSA), accelerates vascular endothelial senescence. Using a CIH mouse model and corresponding cell model, this study examined how molecular hydrogen (H₂) affects endothelial aging. H₂ administration improved aortic pathological changes, restored vasodilatory function, reduced expression of oxidative stress and senescence markers, and elevated autophagy-related protein levels. Echocardiography, aortic ring assays, SA-β-gal staining, DHE staining, and transmission electron microscopy were employed for assessment. Mechanistic experiments showed that Nrf2 silencing diminished H₂'s capacity to attenuate endothelial senescence in the CIH cell model, indicating that H₂ activates mitochondrial autophagy and suppresses oxidative stress through an Nrf2-dependent pathway. These findings provide mechanistic evidence for the potential application of H₂ in OSA-related vascular endothelial aging.
H₂ activates the Nrf2 signaling pathway, which promotes mitochondrial autophagy and reduces CIH-induced oxidative stress, thereby decreasing senescence marker expression and alleviating vascular endothelial cell aging.
This study is at the animal-experiment stage. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/40845957