Abstract
INTRODUCTION: This paper reviews the regulatory effects of hydrogen sulfide (H(2)S) in non-alcoholic fatty liver disease (NAFLD). The research background indicates that NAFLD has become one of the most common chronic liver diseases worldwide, with a complex pathogenesis involving insulin resistance and lipid metabolism disorders. Hydrogen sulfide, as an important gaseous signaling molecule, exerts protective effects in NAFLD through multiple pathways, including antioxidant, anti-inflammatory, lipid metabolism regulation, apoptosis inhibition, and insulin resistance improvement. This article provides a detailed summary of the research overview of NAFLD, the biological characteristics of hydrogen sulfide, its mechanisms of action in NAFLD, empirical studies, and evaluates and prospects current research, aiming to provide a new theoretical basis and experimental support for the treatment of NAFLD. PURPOSE: This literature review aims to systematically synthesize the regulatory roles of hydrogen sulfide (H(2)S) in non-alcoholic fatty liver disease (NAFLD). It provides a comprehensive overview of NAFLD research, the biological characteristics of H(2)S, the mechanisms underlying H(2)S's action in NAFLD, and relevant empirical studies. Additionally, the review evaluates the current state of research and prospects future directions, with the goal of offering novel theoretical foundations and experimental support for NAFLD treatment. PATIENTS AND METHODS: It adopts a comprehensive literature analysis approach. Analyze literature on NAFLD pathogenesis, H(2)S (synthesis/function), and NAFLD treatments (in vitro, animal models, clinical studies). RESULTS: NAFLD links to insulin resistance/inflammation; H(2)S protects against NAFLD by mitigating inflammation, oxidative stress, and lipid accumulation, while improving insulin sensitivity and inhibiting apoptosis. However, its precise mechanisms, stage-specific effects, and therapeutic safety require further clinical validation. CONCLUSION: Hydrogen sulfide (H(2)S), a gaseous signal, exerts multi-mechanistic protective effects in NAFLD. Current limitations include unclear signaling mechanisms and lack of targeted delivery systems. Future research should focus on stage-specific mechanisms, optimized H(2)S donors, and combination therapies for NAFLD treatment.