Endogenous hydrogen sulfide is involved in the pathogenesis of atherosclerosis

Wang, Qiao; Tang, Chaoshu; Jin, Hang; Du, Junbao

doi:10.1016/j.bbrc.2010.04.061

Cited by 56 publications

(32 citation statements)

References 49 publications

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“…Treatment of ApoE knockout mice with NaHS resulted in reduced atherosclerosis plaque, while inhibition of CSE activity enlarged plaque size ). GYY4137, a H 2 S donor, was also shown to decrease aortic atherosclerotic plaque formation and partially restored aortic endothelium-dependent relaxation in ApoE knockout mice (Li et al 2008a;Liu et al 2013;Qiao et al 2010). Another study showed that onion extracts boosted endogenous production of H 2 S and lessened atherosclerotic lesions in rats (Zhang et al 2012a, b).…”

Section: H 2 S and Atherosclerosismentioning

confidence: 92%

H2S and Blood Vessels: An Overview

Yang

Wang

2015

Handbook of Experimental Pharmacology

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The physiological and biomedical importance of hydrogen sulfide (H2S) has been fully recognized in the cardiovascular system as well as in the rest of the body. In blood vessels, cystathionine γ-lyase (CSE) is a major H2S-producing enzyme expressed in both smooth muscle and endothelium as well as periadventitial adipose tissues. Regulation of H2S production from CSE is controlled by a complex integration of transcriptional, posttranscriptional, and posttranslational mechanisms in blood vessels. In smooth muscle cells, H2S regulates cell apoptosis, phenotypic switch, relaxation and contraction, and calcification. In endothelial cells, H2S controls cell proliferation, cellular senescence, oxidative stress, inflammation, etc. H2S interacts with nitric oxide and acts as an endothelium-derived relaxing factor and an endothelium-derived hyperpolarizing factor. H2S generated from periadventitial adipose tissues acts as an adipocyte-derived relaxing factor and modulates the vascular tone. Extensive evidence has demonstrated the beneficial roles of the CSE/H2S system in various blood vessel diseases, such as hypertension, atherosclerosis, and aortic aneurysm. The important roles signaling in the cardiovascular system merit further intensive and extensive investigation. H2S-releasing agents and CSE activators will find their great applications in the prevention and treatment of blood vessel-related disorders.

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Section: H 2 S and Atherosclerosismentioning

confidence: 92%

H2S and Blood Vessels: An Overview

Yang

Wang

2015

Handbook of Experimental Pharmacology

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“…13,14 Because these pathways contribute to the pathophysiology of cardiovascular diseases, it is not surprising that several studies showed cardioprotective effects of H 2 S 15,16 as well as antiatherosclerotic properties. 17,18 In addition, H 2 S plays a role in the regulation of blood pressure through vasorelaxation. 19,20 Recently, the pharmacological profile of a new H 2 Sreleasing aspirin (ACS14) was described.…”

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confidence: 99%

Hydrogen Sulfide–Releasing Aspirin Derivative ACS14 Exerts Strong Antithrombotic Effects In Vitro and In Vivo

Pircher

Fochler²,

Czermak³

et al. 2012

ATVB

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Objective-Hydrogen sulfide (H 2 S)-releasing NSAIDs exert potent anti-inflammatory effects beyond classical cyclooxygenase inhibition. Here, we compared the platelet inhibitory effects of the H 2 S-releasing aspirin derivative ACS14 with its mother compound aspirin to analyze additional effects on platelets. Methods and Results-In platelets of mice fed with ACS14 for 6 days (50 mg/kg per day), not only arachidonic acidinduced platelet aggregation but also ADP-dependent aggregation was decreased, an effect that was not observed with an equimolar dose of aspirin (23 mg/kg per day). ACS14 led to a significantly longer arterial occlusion time after light-dye-induced endothelial injury as well as decreased thrombus formation after ferric chloride-induced injury in the carotid artery. Bleeding time was not prolonged compared with animals treated with equimolar doses of aspirin. In vitro, in human whole blood, ACS14 (25-500 µmol/L) inhibited arachidonic acid-induced platelet aggregation, but compared with aspirin additionally reduced thrombin receptor-activating peptide-, ADP-, and collagen-dependent aggregation. In washed human platelets, ACS14 (500 µmol/L) attenuated αIIbβ3 integrin activation and fibrinogen binding and increased intracellular cAMP levels and cAMP-dependent vasodilator-stimulated phosphoprotein (VASP) phosphorylation. Conclusion-The

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“…NO and H 2 S share several athero-protective actions, including blood vessel relaxation and regulation of vascular tone, EC regeneration, inhibition of leukocyte adhesion, inhibition of platelet clumping to make the blood thinner, and prevention of proliferation and migration of VSMCs [150][151][152][153]. The role of NO in atherosclerosis development has been studied in apolipoprotein E knockout (apoE-KO) mice, where L-NAME treatment significantly decreased NO-mediated vascular response and increased atherosclerosis development [154].…”

Section: The Roles Of H 2 S and No In Atherosclerosismentioning

confidence: 99%

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

Altaany¹,

Moccia²,

Munaron³

et al. 2014

CMC

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The endothelium is a cellular monolayer that lines the inner surface of blood vessels and plays a central role in the maintenance of cardiovascular homeostasis by controlling platelet aggregation, vascular tone, blood fluidity and fibrinolysis, adhesion and transmigration of inflammatory cells, and angiogenesis. Endothelial dysfunctions are associated with various cardiovascular diseases, including atherosclerosis, hypertension, myocardial infarction, and cardiovascular complications of diabetes. Numerous studies have established the antiinflammatory, anti-apoptotic, and anti-oxidant effects of hydrogen sulfide (H 2 S), the latest member to join the gasotransmitter family along with nitric oxide and carbon monoxide, on vascular endothelium. In addition, H 2 S may prime endothelial cells (ECs) toward angiogenesis and contribute to wound healing, aside to its well-known ability to relax vascular smooth muscle cells (VSMCs), thereby reducing blood pressure. Finally, H 2 S may inhibit VSMC proliferation and platelet aggregation. Consistently, a deficit in H 2 S homeostasis is involved in the pathogenesis of atherosclerosis and of hyperglycaemic endothelial injury. Therefore, the application of H 2 S-releasing drugs or using gene therapy to increase endogenous H 2 S level may help restore endothelial function and antagonize the progression of cardiovascular diseases. The present article reviews recent studies on the role of H 2 S in endothelial homeostasis, under both physiological and pathological conditions, and its putative therapeutic applications. Endothelial structure and functionThe endothelium lines the luminal surface of the entire vascular tree and the cardiac chambers, where it is termed endocardium. As a consequence, the endothelium presents a rather broad extension (300 to 1000 m 2 ) and weight (1.5 kg), achieving sizes comparable to other vital organs of the human body [1,2]. The endothelium can, therefore, be regarded as a real "organ spread across the organism" [3] and, as such, not only it is important for the regulation of local tissue functions, but also for maintaining the whole organism homeostasis [4]. Vascular endothelial cells (ECs) possess a polarized architecture: their luminal membrane is directly exposed to hematic constituents and circulating cells, while the basolateral surface is separated from surrounding tissues by a glycoprotein basement membrane -the sub-endothelial basement -which is formed by fibronectin, laminin, and collagen and is secreted by ECs themselves [2].Heterogeneity is, however, the hallmark of endothelium. ECs differ in morphology, function, and gene expression profile, so that even neighbouring cells from the same organ and blood vessel type exhibit distinct features [4]. For instance, vascular ECs may vary in size, shape, thickness and position of the nucleus. Albeit oriented along direction of blood flow, to attenuate the impact of shear stress forces on the vascular wall, microvascular ECs are rather thin (0.1 µm) and spindle-like, whilst their macrovascul...

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Endogenous hydrogen sulfide is involved in the pathogenesis of atherosclerosis

Cited by 56 publications

References 49 publications

H2S and Blood Vessels: An Overview

H2S and Blood Vessels: An Overview

Hydrogen Sulfide–Releasing Aspirin Derivative ACS14 Exerts Strong Antithrombotic Effects In Vitro and In Vivo

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

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