• Inês Mateus and Carina Prip-Buus.
• Institut Cochin, INSERM, CNRS, Université de Paris, Paris, France.
• Eur. J. Clin. Invest. 2022 Mar 1; 52 (3): e13680.

BackgroundFor a long time, hydrogen sulphide (H2 S) was considered only as a toxic gas, inhibiting mitochondrial respiration at the level of cytochrome c oxidase, and an environmental pollutant. Nowadays, H2 S is recognized as the third mammalian gasotransmitter, playing an important role in inflammation, septic shock, ischaemia reperfusion events, cardiovascular disease and more recently in liver physiology and chronic liver diseases such as non-alcoholic fatty liver disease (NAFLD).MethodsThis narrative review is based on literature search using PubMed.ResultsFrom a bioenergetic perspective, H2 S is a very unique molecule, serving as a mitochondrial poison at high concentrations or as an inorganic mitochondrial substrate at low concentrations. By using transgenic animal models to specifically modulate liver H2 S biosynthesis or exogenous compounds that release H2 S, several studies demonstrated that H2 S is a key player in liver glucose and lipid metabolism. Liver H2 S content and biosynthesis were also altered in NAFLD animal models with the in vivo administration of H2 S-releasing molecules preventing the further escalation into non-alcoholic-steatohepatitis. Liver steady-state levels of H2 S, and hence its cell signalling properties, are controlled by a tight balance between its biosynthesis, mainly through the transsulphuration pathway, and its mitochondrial oxidation via the sulphide oxidizing unit. However, studies investigating mitochondrial H2 S oxidation in liver dysfunction still remain scarce.ConclusionsSince H2 S emerges as a key regulator of liver metabolism and metabolic flexibility, further understanding the physiological relevance of mitochondrial H2 S oxidation in liver energy homeostasis and its potential implication in chronic liver diseases are of great interest.© 2021 The Authors. European Journal of Clinical Investigation published by John Wiley & Sons Ltd on behalf of Stichting European Society for Clinical Investigation Journal Foundation.

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