NOD2 contributes to myocardial ischemia/reperfusion injury by regulating cardiomyocyte apoptosis and inflammation

Life Sciences ◽  
2016 ◽  
Vol 149 ◽  
pp. 10-17 ◽  
Author(s):  
Yu Liu ◽  
Hui Yang ◽  
Li-Xin Liu ◽  
Wen Yan ◽  
Hong-Jie Guo ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiomyocyte Apoptosis ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Apoptosis And Inflammation

scholarly journals Renal Denervation Ameliorates Cardiomyocyte Apoptosis in Myocardial Ischemia-reperfusion Injury

2021 ◽  
Author(s):  
Zheng Zhao ◽  
Faquan Li ◽  
Chengzhi Lu ◽  
Yiyao Jiang
Keyword(s):  
Endoplasmic Reticulum ◽  
Myocardial Ischemia ◽  
Endoplasmic Reticulum Stress ◽  
Reperfusion Injury ◽  
Renal Denervation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiomyocyte Apoptosis ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Background: Myocardial ischemia-reperfusion injury (I/R) has been improved with drugs and effective reperfusion, but it still cannot be prevented. We compared the effects of renal denervation (RDN) and angiotensin receptor neprilysin inhibitors (ARNIs) on cardiomyocyte apoptosis after I/R to explore whether RDN can reduce cardiomyocyte apoptosis by improving endoplasmic reticulum stress.Methods: Sixty male specific pathogen free (SPF) Wister rats were randomly divided into six groups.(n=6):(a) normal; (b) sham; (c) I/R; (d) RDN; (e) I/R+RDN and (f) I/R+ARNI. We established the I/R rat model by ligating the left anterior descending artery. Rats were exposed tThe renal artery was exposed and then smeared phenol on the vessel for chemical ablation. The I/R+ARNI group received ARNIs for 2 weeks until killed. We also collected the cardiac tissues and blood serum to determine I/R-related indicators and analyze the potential mechanisms involved.Results: The levels of Norepinephrine (NE), Ang II, and aldosterone (ALD)increased significantly in the I/R group but decreased significantly after RDN and ARNI intervention. The expression of Bax, caspase-3, CHOP, PERK, and ATF4 protein was significantly increased in the I/R group, which compared to other groups, and the level of CHOP, PERK, and ATF4 gene expression increased. After RDN intervention, these expression levels recovered to varying degrees. Conclusion: Our results provide new evidence that RDN ameliorates cardiomyocyte apoptosis in I/R. The effect of RDN may be associated with regulating the endoplasmic reticulum stress PERK/ATF4 signaling pathway.

Helix B Surface Peptide Protects against Acute Myocardial Ischemia-Reperfusion Injury via the RISK and SAFE Pathways in a Mouse Model

Cardiology ◽  
2016 ◽  
Vol 134 (2) ◽  
pp. 109-117 ◽  
Author(s):  
Peng Liu ◽  
Wei You ◽  
Lin Lin ◽  
Yongluan Lin ◽  
Xiuying Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Heart Function ◽  
Ischemia Reperfusion ◽  
Cardiomyocyte Apoptosis ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Gsk 3Β

Objective: This study explores the effects of helix B surface peptide (HBSP) on myocardial infarct size (IS), cardiac function, cardiomyocyte apoptosis and oxidative stress damage in mouse hearts subjected to myocardial ischemia-reperfusion injury (MIRI) and also the mechanisms underlying the effects. Method: Male adult mice were subjected to 45 min of ischemia followed by 2 h of reperfusion; 5 min before the reperfusion, they were treated with HBSP or vehicle. MIRI-induced IS, cardiomyocyte apoptosis and cardiac functional impairment were determined and compared. Western blot analysis was then conducted to elucidate the mechanism of HBSP after treatment. Results: HBSP administration before reperfusion significantly reduced the myocardial IS, decreased cardiomyocyte apoptosis, reduced the activities of superoxide dismutase and malondialdehyde and partially preserved heart function. As demonstrated by the Western blot analysis, HBSP after treatment upregulated Akt/GSK-3β/ERK and STAT-3 phosphorylation; these inhibitors, in turn, weakened the beneficial effects of HBSP. Conclusion: HBSP plays a protective role in MIRI in mice by inhibiting cardiomyocyte apoptosis, reducing the MIRI-induced IS, oxidative stress and improving the heart function after MIRI. The mechanism underlying these effects of HBSP is related to the activation of the RISK (reperfusion injury salvage kinase, Akt/GSK-3β/ERK) and SAFE (STAT-3) pathways.

scholarly journals Histone deacetylase HDAC4 participates in the pathological process of myocardial ischemia-reperfusion injury via MEKK1/JNK pathway by binding to miR-206

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Qingman Li ◽  
Lijie Zhu ◽  
Fangqing Niu ◽  
Qingmin Li ◽  
Che Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological Process ◽  
Cardiomyocyte Apoptosis ◽  
Down Regulation ◽  
Jnk Pathway ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

AbstractHistone deacetylases (HDACs) and microRNAs (miRs) have been reported to exert pivotal roles on the pathogenesis of myocardial ischemia-reperfusion injury (MIRI). Therefore, the present study was performed to define the underlying role of HDAC4 and miR-206 in the pathological process of MIRI. An IRI rat model was established. The interaction between HDAC4 and the promoter region of miR-206 was determined using ChIP, and that between miR-206 and mitogen-activated protein kinase kinase kinase 1 (MEKK1) was determined using dual luciferase reporter gene assay. After the loss- or gain-of-function assay in cardiomyocytes, western blot analysis, RT-qPCR, TUNEL, and ELISA assay were performed to define the roles of HDAC4, miR-206, and MEKK1. Up-regulation of HDAC4 and down-regulation of miR-206 occurred in rat myocardial tissues and cardiomyocytes in MIRI. HDAC4 down-regulation or miR-206 up-regulation contributed to reduced cell apoptosis and the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and malondialdehyde (MDA), while elevating the superoxide dismutase (SOD) and glutathione (GSH) contents. Meanwhile, HDAC4 silencing promoted the expression of miR-206, which targeted and negatively regulated MEKK1. Then inhibition of JNK phosphorylation reduced the cardiomyocyte apoptosis to alleviate MIRI. Coherently, HDAC4 silencing could up-regulate the expression of miR-206 to reduce cardiomyocyte apoptosis and inhibit oxidative stress, and exerting a protective effect on MIRI via the MEKK1/JNK pathway.

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