The role of hydrogen in the prevention and treatment of coronary atherosclerotic heart disease.

Abstract

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.

Mechanism

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.