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The Role of Hydrogen Sulfide on Cardiovascular Homeostasis: An Overview with Update on Immunomodulation

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      Hydrogen sulfide (H 2S), the third endogenous gaseous signaling molecule alongside nitric oxide (NO) and carbon monoxide, is synthesized by multiple enzymes in cardiovascular system. Similar to other gaseous mediators, H 2S has demonstrated a variety of biological activities, including anti-oxidative, anti-apoptotic, pro-angiogenic, vasodilating capacities and endothelial NO synthase modulating activity, and regulates a wide range of pathophysiological processes in cardiovascular disorders. However, the underlying mechanisms by which H 2S mediates cardiovascular homeostasis are not fully understood. This review focuses on the recent progress on functional and mechanistic aspects of H 2S in the inflammatory and immunoregulatory processes of cardiovascular disorders, importantly myocardial ischemia, heart failure, and atherosclerosis. Moreover, we highlight the challenges for developing H 2S-based therapy to modulate the pathological processes in cardiovascular diseases. A better understanding of the immunomodulatory and biochemical functions of H 2S might provide new therapeutic strategies for these cardiovascular diseases.

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      Most cited references 116

      • Record: found
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      Heart Disease and Stroke Statistics-2017 Update: A Report From the American Heart Association.

        • Record: found
        • Abstract: not found
        • Article: not found

        Myocardial reperfusion injury.

          • Record: found
          • Abstract: found
          • Article: not found

          Macrophages in the pathogenesis of atherosclerosis.

           Eli Moore,  Ira Tabas (2011)
          In atherosclerosis, the accumulation of apolipoprotein B-lipoproteins in the matrix beneath the endothelial cell layer of blood vessels leads to the recruitment of monocytes, the cells of the immune system that give rise to macrophages and dendritic cells. Macrophages derived from these recruited monocytes participate in a maladaptive, nonresolving inflammatory response that expands the subendothelial layer due to the accumulation of cells, lipid, and matrix. Some lesions subsequently form a necrotic core, triggering acute thrombotic vascular disease, including myocardial infarction, stroke, and sudden cardiac death. This Review discusses the central roles of macrophages in each of these stages of disease pathogenesis. Copyright © 2011 Elsevier Inc. All rights reserved.

            Author and article information

            1Department of Pharmacology, School of Pharmacy, Fudan University , Shanghai, China
            2State Key Laboratory of Quality Research in Chinese Medicine and School of Pharmacy, Macau University of Science and Technology , Macau, China
            Author notes

            Edited by: Jinsong Bian, National University of Singapore, Singapore

            Reviewed by: Hongfang Jin, Peking University First Hospital, China; Yong Ji, Nanjing Medical University, China

            *Correspondence: Xin-Hua Liu, liuxinhua@ Yi-Zhun Zhu, yzzhu@

            This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology

            Front Pharmacol
            Front Pharmacol
            Front. Pharmacol.
            Frontiers in Pharmacology
            Frontiers Media S.A.
            26 September 2017
            : 8
            5622958 10.3389/fphar.2017.00686
            Copyright © 2017 Pan, Qin, Liu and Zhu.

            This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

            Figures: 4, Tables: 0, Equations: 0, References: 116, Pages: 14, Words: 0
            Funded by: National Natural Science Foundation of China 10.13039/501100001809
            Award ID: 81330080
            Award ID: 81573420
            Award ID: 81673428


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