Effect of S-aspirin, a novel hydrogen-sulfide-releasing aspirin (ACS14), on atherosclerosis in apoE-deficient mice

Zhang, Huili; Guo, Changfa; Zhang, Alian; Fan, Yuqi; Gu, Tao; Wu, Duojiao; Sparatore, Anna; Wang, Changqian

doi:10.1016/j.ejphar.2012.10.005

Cited by 45 publications

(22 citation statements)

References 33 publications

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“…These compounds represent promising avenues for therapies targeted at the downstream signaling events in the JAK-STAT pathway in order to reduce the pro-inflammatory effects of IFN-γ. Other therapies target IFN-γ via alternative signaling pathways, for example, ACS14 (a hydrogen sulphide releasing aspirin) is capable of attenuating the expression of IFN-γ-stimulated CX3 chemokine receptor 1 (CX3CR1) via a peroxisome proliferator-activated receptor-γ-dependent mechanism [48] . Hydrogen sulphide has previously been shown to exert anti-atherogenic effects and its use in ACS14 has been shown to reduce atherosclerosis development in ApoE mice models [48,49] .…”

Section: Resultsmentioning

confidence: 99%

“…Other therapies target IFN-γ via alternative signaling pathways, for example, ACS14 (a hydrogen sulphide releasing aspirin) is capable of attenuating the expression of IFN-γ-stimulated CX3 chemokine receptor 1 (CX3CR1) via a peroxisome proliferator-activated receptor-γ-dependent mechanism [48] . Hydrogen sulphide has previously been shown to exert anti-atherogenic effects and its use in ACS14 has been shown to reduce atherosclerosis development in ApoE mice models [48,49] . IFN-γ neutralization involves the use of a soluble IFN-γR (sIFN-γR) which acts as decoy receptor to prevent the activation of IFN-γR and in turn the phosphorylation of STAT1 in the JAK-STAT pathway, in effect "neutralizing" the IFN-γ.…”

Section: Resultsmentioning

confidence: 99%

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Interferon-γ: Promising therapeutic target in atherosclerosis

Moss

Ramji

2015

WJGEM

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Atherosclerosis is a chronic inflammatory disorder of the vasculature and is the primary cause of cardiovascular disease (CVD). CVD is currently the world's leading cause of death and the numbers are predicted to rise further because of a global increase in risk factors such as diabetes and obesity. Current therapies such as statins have had a major impact in reducing mortality from CVD. However, there is a marked residual CVD risk in patients on statin therapy. It is therefore important to understand the molecular basis of this disease in detail and to develop alternative novel therapeutics. Interferon-γ (IFN-γ) is a pro-inflammatory cytokine that is often regarded as a master regulator of atherosclerosis development. IFN-γ is able to influence several key steps during atherosclerosis development, including pro-inflammatory gene expression, the recruitment of monocytes from the blood to the activated arterial endothelium and plaque stability. This central role of IFN-γ makes it a promising therapeutic target. The purpose of this editorial is to describe the key role IFN-γ plays during atherosclerosis development, as well as discuss potential strategies to target it therapeutically.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Interferon-γ: Promising therapeutic target in atherosclerosis

Moss

Ramji

2015

WJGEM

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“…Combining a tNSAID/coxib with NO or HS donors to provide additional vasodilator activity to offset vascular COX-2 depletion is another possibility for treating chronic pain or inflammation wihout imposing CV risk [53]; a variety of such combination molecules are currently being tested in animal models including NO-Coxibs [54], NO-NSAIDs [55], and NOSH-aspirin [56,57].…”

Section: Effects Of Inhibitors Of Prostanoid Synthesis On Blood Vessementioning

confidence: 99%

Prostanoids and NSAIDs in Cardiovascular Biology and Disease

Weksler

2015

Curr Atheroscler Rep

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Prostanoids and related arachidonic acid derivatives are important physiologic modulators in arteries, as well as mediators of inflammation, hemostasis, and cell proliferation. Their participation in atherosclerosis and in acute thrombotic events is complex, as demonstrated by untoward cardiovascular (CV) effects associated with clinical use of inhibitors of prostaglandin synthesis for treatment of chronic pain, inflammatory states, or cancer prophylaxis. Newer understanding of the pathophysiology of atherosclerosis and the pharmacology of prostanoids promises potential resolution of current problems resulting from the hazards of available prostanoid-altering drugs.

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“…GYY4137 could also dilate arteries [131, 132] and attenuate fibrosis of myocytes [130], which might also be implicated in atherosclerosis prevention [51]. S-aspirin (ACS14), another H 2 S-releasing chemical, also protects 12-week high-fat fed ApoE KO mice from atherosclerosis by 12-week treatment of ACS14 via reducing CX3CR1 expression in lesions and impeding atherogenesis and progress of atherosclerosis [133]. ACS14 also inhibits human platelet aggregation [105] and has strong antithrombotic effects [134].…”

Section: Anti-atherosclerotic Effect Of H2s-releasing Drugsmentioning

confidence: 99%

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

Zj¹,

Wu²,

Guo³

et al. 2017

Cell Physiol Biochem

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Hydrogen sulfide (H₂S) is now admitted as a third gasotransmitter together with nitric oxide (NO) and carbon monoxide (CO), albeit it was originally considered as a foul and poisonous gas. Endogenous H₂S production in mammalian cells is counting on the three enzymes acting on cysteine. Involvement of H₂S in various physiological and pathological processes has been extensively studied in the last fifteen years. Mounting evidence suggests that H₂S is able to protect against atherosclerosis development and progression. Exogenous H₂S supplement has salutary effects on atherogenesis, and reduction of the endogenous H₂S level accelerates atherosclerosis. The anti-atherosclerotic mechanisms of H₂S have been descried in different aspects, including endothelium preservation, antioxidative action, anti-inflammatory responses, vasorelaxation, regulation of ion channels, etc. However, further investigation is still needed to help us gain more insights into the fundamental underlying mechanisms, and that will allow us to design better therapeutic applications of H₂S in the treatment of atherosclerosis.

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Effect of S-aspirin, a novel hydrogen-sulfide-releasing aspirin (ACS14), on atherosclerosis in apoE-deficient mice

Cited by 45 publications

References 33 publications

Interferon-γ: Promising therapeutic target in atherosclerosis

Interferon-γ: Promising therapeutic target in atherosclerosis

Prostanoids and NSAIDs in Cardiovascular Biology and Disease

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

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