Hydrogen Sulfide Actions in the Vasculature

Mendiola, Perenkita J; Naik, Jay S.; Bosc, Laura V. González; Gardiner, Amy S.; Birg, Aleksandr; Kanagy, Nancy L.

doi:10.1002/cphy.c200036

Cited by 7 publications

(6 citation statements)

References 257 publications

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“…Recent studies have confirmed the role of endogenous H 2 S in the activation of mitogen-activated protein kinase cascade. 37 Elevated levels of ERK1/2 and p38 phosphorylation were observed after stimulation of endothelial cells with VEGF, which may be blocked by CSE silencing. The ATP-sensitive potassium channel is the main mediator of the H 2 S effect and is located upstream of p38.…”

Section: H 2 S-related Signaling Pathways In Angiogenesismentioning

confidence: 97%

“…The ATP-sensitive potassium channel is the main mediator of the H 2 S effect and is located upstream of p38. 37 Direct inhibition of endogenous synthesis of H 2 S with pharmacological agents or CSE gene silencing resulted in reduced intracellular cyclic guanosine monophosphate (cGMP) levels, whereas overexpression of CSE upregulated cGMP by direct inhibition of phosphodiesterase activity by H 2 S. 38 In addition, H 2 S production activated the PI3K/Akt signaling pathway, leading to endothelial nitric oxide synthase (eNOS) phosphorylation and eNOS activation. 39 Activation of the PI3K/Akt pathway may result from inhibition of lipid phosphatase and tensin homologue expression by H 2 S. 40 Vasodilator stimulated phosphoprotein phosphorylation at Ser239 was upregulated in endothelial cells treated with L-cysteine, demonstrating that endogenous H 2 S activated the cGMP/PKG pathway.…”

Section: H 2 S-related Signaling Pathways In Angiogenesismentioning

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: H 2 S-related Signaling Pathways In Angiogenesismentioning

confidence: 97%

Section: H 2 S-related Signaling Pathways In Angiogenesismentioning

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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“… 18 , 29 , 30 The lipophilic characteristics of H 2 S and the localization advantage of H 2 S‐producing enzymes together determine that H 2 S plays a vital role in regulating vasodilation, angiogenesis and anti‐endothelial cell senescence. 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 …”

Section: Production and Metabolism Of H 2 ...mentioning

confidence: 99%

“…In addition, the three enzymes can be found in the vascular endothelium 18,29,30 . The lipophilic characteristics of H 2 S and the localization advantage of H 2 S‐producing enzymes together determine that H 2 S plays a vital role in regulating vasodilation, angiogenesis and anti‐endothelial cell senescence 31–39 …”

Section: Production and Metabolism Of H2smentioning

confidence: 99%

“…18,29,30 The lipophilic characteristics of H 2 S and the localization advantage of H 2 Sproducing enzymes together determine that H 2 S plays a vital role in regulating vasodilation, angiogenesis and anti-endothelial cell senescence. [31][32][33][34][35][36][37][38][39] Scavenging mechanism contributes to alleviate toxic effects of H 2 S. H 2 S can be oxidized in mitochondria by the sulphide quinone oxidoreductase system to form thiosulphates and sulphates, or methylated in the cytoplasm by thiol-S-methyltransferase to form dimethyl sulphide and methanethiol. 40,41 It can also be bound by methaemoglobin to produce Sul haemoglobin, which is excreted by spleen.…”

Section: Production and Metabolism Of H Smentioning

confidence: 99%

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Role of hydrogen sulphide in physiological and pathological angiogenesis

et al. 2022

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The role of hydrogen sulphide (H2S) in angiogenesis has been widely demonstrated. Vascular endothelial growth factor (VEGF) plays an important role in H2S‐induced angiogenesis. H2S promotes angiogenesis by upregulating VEGF via pro‐angiogenic signal transduction. The involved signalling pathways include the mitogen‐activated protein kinase pathway, phosphoinositide‐3 kinase pathway, nitric oxide (NO) synthase/NO pathway, signal transducer and activator of transcription 3 (STAT3) pathway, and adenosine triphosphate (ATP)‐sensitive potassium (KATP) channels. H2S has been shown to contribute to tumour angiogenesis, diabetic wound healing, angiogenesis in cardiac and cerebral ischaemic tissues, and physiological angiogenesis during the menstrual cycle and pregnancy. Furthermore, H2S can exert an anti‐angiogenic effect by inactivating Wnt/β‐catenin signalling or blocking the STAT3 pathway in tumours. Therefore, H2S plays a double‐edged sword role in the process of angiogenesis. The regulation of H2S production is a promising therapeutic approach for angiogenesis‐associated diseases. Novel H2S donors and/or inhibitors can be developed in the treatment of angiogenesis‐dependent diseases.

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