分子状水素が心血管系および中枢神経系に及ぼす分子・細胞メカニズムに関するレビュー
Excess reactive oxygen species and oxidative stress are central contributors to pathology in the cardiovascular and central nervous systems. This review consolidates experimental and clinical evidence on how molecular hydrogen (H2) influences these systems at the molecular and cellular levels. Key areas examined include redox and intracellular signaling regulation, changes in gene expression, and modulation of cellular processes such as autophagy, apoptosis, and tissue remodeling. The review highlights H2 as a regulator of Nrf2-mediated redox signaling and identifies mitochondria as a principal target of its action. Connections between H2's antioxidant functions and protein kinase signaling—particularly the PI3K/Akt and Wnt/β-catenin pathways—are discussed, with attention to glycogen synthase kinase 3β and its role in apoptosis regulation. The modulation of autophagy and matrix metalloproteinase-driven tissue remodeling by H2 is also addressed.
H2 activates Nrf2-mediated antioxidant signaling, modulates apoptosis via PI3K/Akt and Wnt/β-catenin pathways through GSK3β regulation, protects mitochondrial function, and influences autophagy as well as matrix metalloproteinase-driven tissue remodeling in response to cellular stress.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (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/33333951