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The double-edged role of hydrogen sulfide in the pathomechanism of multiple liver diseases
Summary
This review examined the double-edged role of hydrogen sulfide (H2S) as a gaseous signaling molecule across multiple liver disease conditions, summarizing its protective antioxidant and anti-inflammatory effects alongside its potential to exacerbate damage at higher concentrations. The findings suggest context-dependent therapeutic windows for H2S modulation in liver disease.
In mammalian systems, hydrogen sulfide (H2S)-one of the three known gaseous signaling molecules in mammals-has been found to have a variety of physiological functions. Existing studies have demonstrated that endogenous H2S is produced through enzymatic and non-enzymatic pathways. The liver is the body's largest solid organ and is essential for H2S synthesis and elimination. Mounting evidence suggests H2S has essential roles in various aspects of liver physiological processes and pathological conditions, such as hepatic lipid metabolism, liver fibrosis, liver ischemia‒reperfusion injury, hepatocellular carcinoma, hepatotoxicity, and acute liver failure. In this review, we discuss the functions and underlying molecular mechanisms of H2S in multiple liver pathophysiological conditions.
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