The Role of Hydrogen Sulfide Regulation of Autophagy in Liver Disorders

Lü, Xueqin; Ding, Yueming; Liu, Huiyang; Sun, Mengyao; Chen, Chaoran; Yang, Yihan; Wang, Honggang

doi:10.3390/ijms23074035

Cited by 10 publications

(6 citation statements)

References 99 publications

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“…19,20 Interaction between hypoxia and H 2 S H 2 S is believed to be the third gaseous signaling molecule which is widely expressed in mammalian cells and tissues. 21 Three enzymes are known to be involved in the production of endogenous H 2 S, namely cystathionine beta synthase (CBS), cystathionine gamma lyase (CSE), and 3-Mercaptopyruvate sulfotransferase (3-MST). 9 An increasing body of evidence has revealed the cross-talk between HIF-1 and H 2 S. In a study, knockdown of CSE was shown to affect H 2 S production, which impaired the stability of HIF-1α, suggesting that endogenous H 2 S is important for the regulation of HIF-1 signaling pathway.…”

Section: Adaptive Changes In Hhmementioning

confidence: 99%

“…49 In addition to causing endothelial dysfunction, homocysteine has been shown to cause contraction of HSC. This homocysteine-induced contraction of HSC is reversed by H 2 S. 21 HSC contraction is associated with regulation of liver sinusoidal blood flow and intrahepatic resistance, and it is hypothesized that H 2 S may be involved in regulating HSC contraction together with LSEC-derived paracrine cytokines. 21 Briefly, reduced levels of H 2 S in the portal microcirculation cause an increase in intrahepatic resistance, not only because it is part of endothelial dysfunction, but also because it facilitates the activation and contraction of HSC.…”

Section: Vasodilatory Effects Of H 2 S In Portal Hypertensionmentioning

confidence: 99%

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Role of Hydrogen Sulfide and Hypoxia in Hepatic Angiogenesis of Portal Hypertension

Yang¹,

Tan²,

Gao³

et al. 2023

J Clin Transl Hepatol

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The pathogenesis of portal hypertension remains unclear, and is believed to involve dysfunction of liver sinusoidal endothelial cells (LSEC), activation of hepatic stellate cells (HSC), dysregulation of endogenous hydrogen sulfide (H 2 S) synthesis, and hypoxia-induced angiogenic responses. H 2 S, a novel gas transmitter, plays an important role in various pathophysiological processes, especially in hepatic angiogenesis. Inhibition of endogenous H 2 S synthase by pharmaceutical agents or gene silencing may enhance the angiogenic response of endothelial cells. Hypoxia-inducible factor-1 (HIF-1) is the main transcription factor of hypoxia, which induces hepatic angiogenesis through up-regulation of vascular endothelial growth factor (VEGF) in HSC and LSEC. H 2 S has also been shown to be involved in the regulation of VEGF-mediated angiogenesis. Therefore, H 2 S and HIF-1 may be potential therapeutic targets for portal hypertension. The effects of H 2 S donors or prodrugs on the hemodynamics of portal hypertension and the mechanism of H 2 S-induced angiogenesis are promising areas for future research.

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Section: Adaptive Changes In Hhmementioning

confidence: 99%

Section: Vasodilatory Effects Of H 2 S In Portal Hypertensionmentioning

confidence: 99%

Role of Hydrogen Sulfide and Hypoxia in Hepatic Angiogenesis of Portal Hypertension

Yang¹,

Tan²,

Gao³

et al. 2023

J Clin Transl Hepatol

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“…In addition, L-cystine can be converted into 3-mercaptopyruvate (3-MP) catalyzed by cysteine aminotransferase (CAT) by transferring amine to α-ketoglutarate to form 3-mercaptopyruvate (3-MP). Finally, 3-MP can be converted into H 2 S catalyzed by 3-MST (Figure 2) [32][33][34]. Studies have shown that H 2 S is involved in various physiological processes, including inflammatory response, energy metabolism, oxidative stress, mitochondrial biogenesis, and neuroregulation [35][36][37][38].…”

Section: Overview Of Hydrogen Sulfidementioning

confidence: 99%

Hydrogen Sulfide Plays an Important Role by Regulating Endoplasmic Reticulum Stress in Diabetes-Related Diseases

Zhao

Liu

Yang

et al. 2022

IJMS

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Endoplasmic reticulum (ER) plays important roles in protein synthesis, protein folding and modification, lipid biosynthesis, calcium storage, and detoxification. ER homeostasis is destroyed by physiological and pharmacological stressors, resulting in the accumulation of misfolded proteins, which causes ER stress. More and more studies have shown that ER stress contributes to the pathogenesis of many diseases, such as diabetes, inflammation, neurodegenerative diseases, cancer, and autoimmune diseases. As a toxic gas, H2S has, in recent years, been considered the third most important gas signal molecule after NO and CO. H2S has been found to have many important physiological functions and to play an important role in many pathological and physiological processes. Recent evidence shows that H2S improves the body’s defenses to many diseases, including diabetes, by regulating ER stress, but its mechanism has not yet been fully understood. We therefore reviewed recent studies of the role of H2S in improving diabetes-related diseases by regulating ER stress and carefully analyzed its mechanism in order to provide a theoretical reference for future research.

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“…After carbon monoxide (CO) and nitrous oxide (NO), hydrogen sulfide (H 2 S) is the third gaseous signal molecule associated with smooth muscle relaxation in the vascular system [ 67 ]. H 2 S has other important biological functions and is involved in various human diseases, including MAFLD [ 68 ].…”

Section: Autophagy In Mafldmentioning

confidence: 99%

Autophagy Dysregulation in Metabolic Associated Fatty Liver Disease: A New Therapeutic Target

Chen

Lin

2022

IJMS

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Metabolic associated fatty liver disease (MAFLD) is one of the most common causes of chronic liver disease worldwide. To date, there is no FDA-approved treatment, so there is an urgent need to determine its pathophysiology and underlying molecular mechanisms. Autophagy is a lysosomal degradation pathway that removes damaged organelles and misfolded proteins after cell injury through endoplasmic reticulum stress or starvation, which inhibits apoptosis and promotes cell survival. Recent studies have shown that autophagy plays an important role in removing lipid droplets from hepatocytes. Autophagy has also been reported to inhibit the production of pro-inflammatory cytokines and provide energy for the hepatic stellate cells activation during liver fibrosis. Thyroid hormone, irisin, melatonin, hydrogen sulfide, sulforaphane, DA-1241, vacuole membrane protein 1, nuclear factor erythroid 2-related factor 2, sodium-glucose co-transporter type-2 inhibitors, immunity-related GTPase M, and autophagy-related gene 7 have been reported to ameliorate MAFLD via autophagic induction. Lipid receptor CD36, SARS-CoV-2 Spike protein and leucine aminopeptidase 3 play a negative role in the autophagic function. This review summarizes recent advances in the role of autophagy in MAFLD. Autophagy modulates major pathological changes, including hepatic lipid metabolism, inflammation, and fibrosis, suggesting the potential of modulating autophagy for the treatment of MAFLD.

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The Role of Hydrogen Sulfide Regulation of Autophagy in Liver Disorders

Cited by 10 publications

References 99 publications

Role of Hydrogen Sulfide and Hypoxia in Hepatic Angiogenesis of Portal Hypertension

Role of Hydrogen Sulfide and Hypoxia in Hepatic Angiogenesis of Portal Hypertension

Hydrogen Sulfide Plays an Important Role by Regulating Endoplasmic Reticulum Stress in Diabetes-Related Diseases

Autophagy Dysregulation in Metabolic Associated Fatty Liver Disease: A New Therapeutic Target

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