冠動脈アテローム性心疾患における水素の役割：炎症・糖脂質代謝への影響と分子メカニズムのレビュー
Coronary atherosclerotic heart disease (CHD), driven by chronic inflammation and oxidative lipid deposition, represents a major cardiovascular burden. This review examines the potential of molecular hydrogen (H₂) to counteract CHD-related pathology through multiple mechanisms. H₂ is reported to modulate inflammatory signaling via the NF-κB pathway, pyroptosis, mitophagy, endoplasmic reticulum stress, and the Nrf2 antioxidant pathway. In parallel, H₂ may normalize glycolipid metabolism through PI3K and AMPK signaling, thereby potentially limiting CHD progression. The review systematically outlines CHD pathogenesis, evaluates available evidence on H₂ efficacy, and proposes mechanistic hypotheses intended to guide future experimental and clinical investigations.
H₂ is proposed to suppress CHD-related inflammation by modulating NF-κB, pyroptosis, mitophagy, and ER stress pathways, while improving glycolipid metabolism via PI3K and AMPK signaling, with additional antioxidant effects mediated through Nrf2 activation.
The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/38615891