Objective: Hydrogen sulfide (H 2 S) has been reported to be a gasotransmitter which regulates cardiovascular homeostasis. The present study aims to examine the hypothesis that hydrogen sulfide is able to promote angiogenesis. Methods: Angiogenesis was assessed using in vitro parameters (i.e. endothelial cell proliferation, adhesion, transwell migration assay, scratched wound healing and formation of tube-like structure) and in vivo by assessing neovascularization in mice. Phosphorylation of Akt was measured using Western blot analysis. Results: Exogenously administered NaHS (H 2 S donor) concentration-dependently (10-20 μmol/l) increased cell growth, migration, scratched wound healing and tube-like structure formation in cultured endothelial cells. These effects of NaHS on endothelial wound healing and tube-like structure formation were prevented by either the phosphatidylinositol 3-kinase (PI3K) inhibitor LY 294002 (5 μmol/l) or transfection of a dominant-negative mutant of Akt. NaHS increased Akt phosphorylation and this effect was also blocked by either LY 294002 or wortmannin (25 nmol/l). NaHS did not significantly alter the levels of vascular endothelial growth factor, mRNA expression of fibroblast growth factor and angiopoietin-1, or nitric oxide metabolites. NaHS treatment (10 and 50 μmol kg − 1 day − 1 ) significantly promoted neovascularization in vivo in mice. Conclusion:The present study reports a novel proangiogenic role of H 2 S which is dependent on activation of Akt.

H(2)S is a novel inhibitor of L-type calcium channels in cardiomyocytes. Moreover, H(2)S-induced inhibition of [Ca(2+)]i appears to be a secondary effect owing to its initial action towards I(Ca,L). The inhibitory effect of H(2)S on I(Ca,L) requires further investigation, particularly in the exploration of new pathways involved in cardiac calcium homeostasis and disease pathology.

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Since the outbreak of severe acute respiratory syndrome (SARS) in 2003, the harm caused by coronaviruses to the world cannot be underestimated. Recently, a novel coronavirus (severe acute respiratory syndrome coronavirus‐2 [SARS‐CoV‐2]) initially found to trigger human severe respiratory illness in Wuhan City of China in 2019, has infected more than six million people worldwide by 21 June 2020, and which has been recognized as a public health emergency of international concern as well. And the virus has spread to more than 200 countries around the world. However, the effective drug has not yet been officially licensed or approved to treat SARS‐Cov‐2 and SARS‐Cov infection. NSP12‐NSP7‐NSP8 complex of SARS‐CoV‐2 or SARS‐CoV, essential for viral replication and transcription, is generally regarded as a potential target to fight against the virus. According to the NSP12‐NSP7‐NSP8 complex (PDB ID: 7BW4) structure of SARS‐CoV‐2 and the NSP12‐NSP7‐NSP8 complex (PDB ID: 6NUR) structure of SARS‐CoV, NSP12‐NSP7 interface model, and NSP12‐NSP8 interface model were established for virtual screening in the present study. Eight compounds (Nilotinib, Saquinavir, Tipranavir, Lonafarnib, Tegobuvir, Olysio, Filibuvir, and Cepharanthine) were selected for binding free energy calculations based on virtual screening and docking scores. All eight compounds can combine well with NSP12‐NSP7‐NSP8 in the crystal structure, providing drug candidates for the treatment and prevention of coronavirus disease 2019 and SARS.

Suppressed CSE-catalyzed endogenous H(2)S production in the kidney by hyperglycemia may play an important role in the pathogenesis of DN.

SUMMARY1. Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor. Angiotensin AT 1 receptor antagonism has been considered as a specific approach to block the renin-angiotensin system and been demonstrated to be able to prevent or regress LVH by interfering with the remodelling process of the heart. 2. Angiotensin AT 1 receptor blockade induces a marked increase in angiotensin (Ang) II, which may stimulate the AT 2 receptors. Gene expression of AT 1 and AT 2 receptors increases in a time-dependent manner in cardiac remodelling following myocardial infarction.3. Considerable efforts have been made to clarify the role of AT 2 receptors in cardiac hypertrophy and remodelling since the mid-1990s, resulting in controversial reports: the AT 2 receptor mediates actions either opposite to or in coordination with those of the AT 1 receptor. Moreover, there are many reports of no significant effects mediated by AT 2 receptors. 4. Based on the studies reviewed in the present article, we assume that the predominant effect of AngII in cardiac hypertrophy and cardiac remodelling is growth promoting and that this effect is mediated mainly via AT 1 receptors. The AT 2 receptors may affect the hypertrophic process by interacting with other cardiac membrane proteins, enzymes and autacoids. Before coming to a conclusion as to whether AT 2 receptor stimulation or antagonism is beneficial to the heart, more studies should be performed in different LVH models, especially long-term treatment protocols in vivo .

. Chronic sodium hydrosulfide treatment decreases medial thickening of intramyocardial coronary arterioles, interstitial fibrosis, and ROS production in spontaneously hypertensive rats. Am J Physiol Heart Circ Physiol 293: H2093-H2100, 2007. First published July 13, 2007; doi:10.1152/ajpheart.00088.2007.-Hydrogen sulfide (H2S) is a gasotransmitter that regulates cardiovascular functions. The present study aimed to examine the hypothesis that chronic treatment with sodium hydrosulfide (NaHS, an H2S donor) is able to prevent left-ventricular remodeling in spontaneously hypertensive rats (SHR). Four-week-old SHR were treated with NaHS (10, 30, and 90 ), and placebo for 3 mo. At the end of the treatment period, variables such as cardiac geometry and function, intramyocardial arterioles ranging in diameter from 25 to 100 m, perivascular and interstitial collagen content, reactive oxygen species (ROS), thiol groups, conjugated dienes, and DNA base modification were examined. The novel finding of the present study is that chronic NaHS treatment prevented the hypertrophy of intramyocardial arterioles and ventricular fibrosis, as well as decreased myocardial ROS and conjugated diene levels. The cardioprotective effects were blunted by coadministration of glibenclamide, suggesting a role of ATP-sensitive potassium channels in mediating the action of NaHS. Hydralazine caused a comparable reduction of blood pressure compared with NaHS treatment; however, it exerted no effect on the remodeling process or on ROS and conjugated diene levels. Moreover, NaHS treatment caused an increase in myocardial thiol group levels, whereas DNA base modification was not altered by NaHS treatment. In conclusion, the superior cardioprotective effects of NaHS treatment are worthy to be further explored to develop novel therapeutic approaches for the treatment of cardiac remodeling in hypertension.left-ventricular remodeling; gasotransmitter; hypertension; hydrogen sulfide HYPERTENSION-INDUCED left-ventricular hypertrophy is recognized as an independent risk factor for myocardial ischemia, dysfunction, infarction, and heart failure (26). Structural remodeling of coronary arterioles and extracellular matrix becomes obvious in hypertrophied left ventricle (LV) in 4-mo-old spontaneously hypertensive rats (SHR) (15). Hypertension-induced medial thickening of intramyocardial coronary arterioles results in stenosis of the coronary arterioles and consequent myocardial ischemia and dysfunction (19), whereas perivascular fibrosis may induce a compression on the coronary arterioles and therefore account for a reduction in coronary vasodilator reserve. Moreover, an accumulation of fibrillar collagen in the interstitial space of hypertrophied myocardium has been held responsible for abnormal ventricular wall stiffness and for impaired cardiac pumping capacity (12,20). In this context, the aim of antihypertensive therapy is not only to decrease blood pressure (BP) but also to reduce hypertrophy of intramyocardial coronary arterioles and left-ventricular inte...