Exploring the Potential of Molecular Hydrogen in Different Heart Failure Models: A Review

Abstract

Heart failure (HF) is increasing in prevalence in many countries around the world. HF is a complex clinical syndrome characterized by the heart’s inability to pump blood effectively, resulting in significant morbidity and mortality. After an initial cardiac event (e.g., myocardial infarction, valve dysfunction, hypertension, etc.), adaptive mechanisms are activated to preserve cardiac function. Sustained activation of these mechanisms leads to cellular and structural changes involving cardiac remodeling and hypertrophy. This ultimately leads to impaired cardiac contractility and reduced cardiac output, with a 5-year HF-associated mortality rate up to 75%. The current treatment strategies for HF are not sufficient to cover all the underlying complex mechanisms. It has been demonstrated that molecular hydrogen (H2) exerts cardioprotective effects via its antioxidant, anti-inflammatory, and anti-apoptotic action. The number of studies exploring beneficial effects of H2 in different HF models is increasing. This is the first review summarizing the knowledge in this field. The available literature indicates that H2 may be effective in mitigating different HF pathologies via regulating cardiac oxidative stress and inflammation, cardiomyocyte death, and mitochondrial function/cell metabolism, as well as cardiac remodeling, including hypertrophy and fibrosis. As this area of research is still in its infancy, the feasibility and efficiency of H2 treatment in different HF types need further investigation.

Study details

Article type

Review

Disease / injury model

Heart Failure (various models: isoproterenol, aortic constriction, monocrotaline, doxorubicin, genetic models)

Dose comparison

Some studies compared different doses of hydrogen-rich saline (e.g., 3 mL/kg vs. 6 mL/kg) and found dose-dependent effects on cardiac hypertrophy and fibrosis.

Dose-dependent effect

Yes

Outcome

Positive

Findings

Molecular hydrogen (H2) shows promise as a cardioprotective agent in various heart failure (HF) models, exerting antioxidant, anti-inflammatory, anti-apoptotic, anti-hypertrophic, and anti-fibrotic effects. H2 mitigates cardiac oxidative stress, inflammation, cell death, and improves mitochondrial function and cardiac remodeling. However, clinical evidence is still limited and further research is needed to establish efficacy and safety.