Mitochondria-targeted hydrogen sulfide donor reduces atherogenesis by changing macrophage phenotypes and increasing UCP1 expression in vascular smooth muscle cells.

Atherosclerosis is a leading cause of morbidity and mortality in the Western countries. Mounting evidence points to the role of mitochondrial dysfunction in the pathogenesis of atherosclerosis. Recently, it has been shown that mitochondrial hydrogen sulfide (HS) can complement the bioenergetic role of Krebs cycle leading to improved mitochondrial function.

Mitochondria-targeted hydrogen sulfide donor reduces fatty liver and obesity in mice fed a high fat diet by inhibiting de novo lipogenesis and inflammation via mTOR/SREBP-1 and NF-κB signaling pathways.

Metabolic diseases that include obesity and metabolic-associated fatty liver disease (MAFLD) are a rapidly growing worldwide public health problem. The pathogenesis of MAFLD includes abnormally increased lipogenesis, chronic inflammation, and mitochondrial dysfunction. Mounting evidence suggests that hydrogen sulfide (HS) is an important player in the liver, regulating lipid metabolism and mitochondrial function.

The Hydrogen Sulfide Donor AP39 Reduces Glutamate-mediated Excitotoxicity in a Rat Model of Brain Ischemia.

The vast majority of stroke cases are classified as ischemic stroke, but effective pharmacotherapy strategies to treat brain infarction are still limited. Glutamate, which is a primary mediator of excitotoxicity, contributes to neuronal damage in numerous pathologies, including ischemia. The aim of this study was to investigate the effect of the hydrogen sulfide donor AP39 on excitotoxicity.

The mitochondria-targeted sulfide delivery molecule attenuates drugs-induced gastropathy. Involvement of heme oxygenase pathway.

Hydrogen sulfide (HS) signaling and HS-prodrugs maintain redox balance in gastrointestinal (GI) tract. Predominant effect of any HS-donor is mitochondrial. Non-targeted HS-moieties were shown to decrease the non-steroidal anti-inflammatory drugs (NSAIDs)-induced gastrotoxicity but in high doses.

Mitochondrial sulfide promotes life span and health span through distinct mechanisms in developing versus adult treated .

Living longer without simultaneously extending years spent in good health ("health span") is an increasing societal burden, demanding new therapeutic strategies. Hydrogen sulfide (HS) can correct disease-related mitochondrial metabolic deficiencies, and supraphysiological HS concentrations can pro health span. However, the efficacy and mechanisms of mitochondrion-targeted sulfide delivery molecules (mtHS) administered across the adult life course are unknown.