慢性腎臓病における酸化ストレスおよびレドックスシグナルに対する分子状水素の潜在的役割：レビュー
Chronic kidney disease (CKD) progression is closely linked to oxidative stress, which drives renal cell injury, inflammatory responses, and fibrotic changes. Molecular hydrogen (H2) exhibits selective scavenging of hydroxyl radicals and peroxynitrite while preserving physiologically necessary reactive oxygen species. This review examines how H2 modulates multiple redox-related signaling networks relevant to CKD. Activation of the NRF2-KEAP1 axis by H2 strengthens antioxidant defenses; this effect is further amplified through the Wnt/β-catenin pathway and indirect mitochondrial NRF2-KEAP1 engagement. H2 also regulates NF-κB activity via cellular redox modulation, suppresses MAPK cascades, sustains thioredoxin levels, attenuates HIF signaling by neutralizing ROS, and influences FOXO transcription factors alongside antioxidant enzyme activity. Although preclinical findings are encouraging, clinical evidence remains sparse, and the authors call for expanded trials to clarify H2's role in renal oxidative stress management.
H2 selectively neutralizes hydroxyl radicals and peroxynitrite, activates the NRF2-KEAP1 antioxidant axis (including via Wnt/β-catenin and mitochondrial pathways), suppresses NF-κB and MAPK signaling, modulates HIF and FOXO factors, and enhances antioxidant enzyme activity, collectively reducing renal oxidative 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/38795643