scholarly journals Two Novel Approaches Providing Cardiac Protection Against Oxidative Stress

10.5772/31890 ◽  
2012 ◽  
Author(s):  
Howard Prentice ◽  
Herbert Weissbach
Keyword(s):  
Oxidative Stress ◽  
Cardiac Protection ◽  
Novel Approaches

Abstract 265: Uroetensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through Cystathionine-γ-Lyase (CSE)/Hydrogen Sulfide Pathway

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Hui Gong ◽  
Zhidan Chen ◽  
Xiaoyi Zhang ◽  
Jie Zhang ◽  
Yang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Erk Signaling ◽  
Cardiac Protection ◽  
Health Control ◽  
Cardiology Department ◽  
Apoptotic Protein ◽  
Induced Apoptosis ◽  
H2s Production

Plasma UII has been observed to be raised in patients with acute myocardial infarction, a lower UII response is associated with more severe injury of myocardium, suggesting a possible cardioprotective role for this peptide. In the present study, we studied plasma UII concentration of thirty patients admitted to the Cardiology Department with acute myocardial infartion.The results showed that plasma UII was sharply increased in patients compared to that in health control within one week after admission. We then explore whether UII could protect cardiomyocytes from injury induced by oxidative stress. Cultured cardiomyocyte were treated with H2O2 to induce oxidative stress, and the influence of UII on H2O2-induced apoptosis was observed. The results showed that UII pretreatment significantly reduced the number of TUNEL-positive cardiomyocytes induced by H2O2, and it partly abolished the upregulation of pro-apoptotic protein Bax and the down-regulation of anti-apoptotic protein Bcl-2. siRNA targeted to urotensin receptor (UT) greatly inhibited these effects. H2S has been reported to exert protective effect on cardiomyocytes, we detected the effect of UII on H2S production and CSE (Major H2S-producing enzyme) expressions in cardiomyocytes exposed to H2O2.The present data revealed that UII increased the H2S production by enhancing the expression of CSE by activating the ERK signaling in cardiomyocytes exposed to H2O2. Si-CSE or ERK inhibitor not only greatly inhibited the upregulation of CSE or the phosphorylation of ERK induced by UII but also reversed UII-induced-upregulation of H2S production and anti-apoptosis in cadiomyocytes exposed to H2O2. In conclusion, UII rapidly promoted the phosphorylation of ERK, increased CSE exression and induced H2S production, which in turn enhanced the p-ERK level to protect cardiomyocytes from apoptosis under ischemic or oxidative stress. The increased plasma UII level in patients may be critical for cardiac protection in patients at early-phase of acute myocardial infarction.

scholarly journals Biomarkers of oxidative and nitro-oxidative stress: conventional and novel approaches

2017 ◽  
Vol 174 (12) ◽  
pp. 1771-1783 ◽  
Author(s):  
Ana Cipak Gasparovic ◽  
Neven Zarkovic ◽  
Kamelija Zarkovic ◽  
Khrystyna Semen ◽  
Danylo Kaminskyy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Novel Approaches

scholarly journals Recent novel approaches to limit oxidative stress and inflammation in diabetic complications

2018 ◽  
Vol 7 (4) ◽  
pp. e1016 ◽  
Author(s):  
Raelene J Pickering ◽  
Carlos J Rosado ◽  
Arpeeta Sharma ◽  
Shareefa Buksh ◽  
Mitchel Tate ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Complications ◽  
Novel Approaches

scholarly journals Physiological and Pharmacological Roles of FGF21 in Cardiovascular Diseases

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Peng Cheng ◽  
Fangfang Zhang ◽  
Lechu Yu ◽  
Xiufei Lin ◽  
Luqing He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Development ◽  
Fibroblast Growth Factor 21 ◽  
Therapeutic Effects ◽  
Fibroblast Growth ◽  
Mechanistic Studies ◽  
Cardiac Protection ◽  
Compensatory Response ◽  
Beneficial Effects ◽  
Cardiac Lipotoxicity

Cardiovascular disease (CVD) is one of the most severe diseases in clinics. Fibroblast growth factor 21 (FGF21) is regarded as an important metabolic regulator playing a therapeutic role in diabetes and its complications. The heart is a key target as well as a source of FGF21 which is involved in heart development and also induces beneficial effects in CVDs. Our review is to clarify the roles of FGF21 in CVDs. Strong evidence showed that the development of CVDs including atherosclerosis, coronary heart disease, myocardial ischemia, cardiac hypertrophy, and diabetic cardiomyopathy is associated with serum FGF21 levels increase which was regarded as a compensatory response to induced cardiac protection. Furthermore, administration of FGF21 suppressed the above CVDs. Mechanistic studies revealed that FGF21 induced cardiac protection likely by preventing cardiac lipotoxicity and the associated oxidative stress, inflammation, and apoptosis. Normally, FGF21 induced therapeutic effects against CVDs via activation of the above kinases-mediated pathways by directly binding to the FGF receptors of the heart in the presence ofβ-klotho. However, recently, growing evidence showed that FGF21 induced beneficial effects on peripheral organs through an indirect way mediated by adiponectin. Therefore whether adiponectin is also involved in FGF21-induced cardiac protection still needs further investigation.

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