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https://www.readbyqxmd.com/read/28298952/insights-for-oxidative-stress-and-mtor-signaling-in-myocardial-ischemia-reperfusion-injury-under-diabetes
#1
REVIEW
Dajun Zhao, Jian Yang, Lifang Yang
Diabetes mellitus (DM) displays a high morbidity. The diabetic heart is susceptible to myocardial ischemia/reperfusion (MI/R) injury. Impaired activation of prosurvival pathways, endoplasmic reticulum (ER) stress, increased basal oxidative state, and decreased antioxidant defense and autophagy may render diabetic hearts more vulnerable to MI/R injury. Oxidative stress and mTOR signaling crucially regulate cardiometabolism, affecting MI/R injury under diabetes. Producing reactive oxygen species (ROS) and reactive nitrogen species (RNS), uncoupling nitric oxide synthase (NOS), and disturbing the mitochondrial quality control may be three major mechanisms of oxidative stress...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28292026/catalpol-protects-glucose-deprived-rat-embryonic-cardiac-cells-by-inducing-mitophagy-and-modulating-estrogen-receptor
#2
Chao Lin, Ying Lu, Xiaojing Yan, Xiang Wu, Meiyu Kuai, Xin Sun, Qi Chen, Xueyun Kong, Zhaoguo Liu, Yuping Tang, Yi Jing, Yu Li, Qichun Zhang, Huimin Bian
Catalpol, a bioactive component from Rehmannia glutinosa (Di Huang), has been widely used to protect cardiomyocytes against myocardial ischemia. The aim of the present study was to investigate the anti-apoptotic and anti-oxidative effects of Catalpol on glucose-starved H9c2 cells for cardio-protection and to elucidate the underlying mechanisms. Here, we showed that Catalpol protected the glucose-starved H9c2 cells through reducing apoptosis and attenuating oxidative damage. Moreover, the increases of autophagic lysosomes, LC3, autophagic flux and autophagic vacuole were observed in Catalpol-treated cells using flow cytometer and fluorescence microscope...
March 9, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28287478/myocardial-ischemic-postconditioning-promotes-autophagy-against-ischemia-reperfusion-injury-via-the-activation-of-the-nnos-ampk-mtor-pathway
#3
Maojuan Hao, Suhua Zhu, Liang Hu, Hongyi Zhu, Xiaowei Wu, Qingping Li
Autophagy participates in the progression of many diseases, comprising ischemia/ reperfusion (I/R). It is reported that it is involved in the protective mechanism of ischemic postconditioning (IPostC). According to research, neuronal nitric oxide synthase (nNOS) is also involved in the condition of I/R and IPostC. However, the relationship between nNOS, autophagy and IPostC has not been previously investigated. We hypothesize that IPostC promotes autophagy activity against I/R injury partially through nNOS-mediated pathways...
March 11, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28265179/n-acetylcysteine-attenuates-diabetic-myocardial-ischemia-reperfusion-injury-through-inhibiting-excessive-autophagy
#4
Sheng Wang, Chunyan Wang, Fuxia Yan, Tingting Wang, Yi He, Haobo Li, Zhengyuan Xia, Zhongjun Zhang
Background. Excessive autophagy is a major mechanism of myocardial ischemia reperfusion injury (I/RI) in diabetes with enhanced oxidative stress. Antioxidant N-acetylcysteine (NAC) reduces myocardial I/RI. It is unknown if inhibition of autophagy may represent a mechanism whereby NAC confers cardioprotection in diabetes. Methods and Results. Diabetes was induced in Sprague-Dawley rats with streptozotocin and they were treated without or with NAC (1.5 g/kg/day) for four weeks before being subjected to 30-minute coronary occlusion and 2-hour reperfusion...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28260802/autophagy-inhibitor-3-methyladenine-alleviates-overload-exercise-induced-cardiac-injury-in-rats
#5
Hua Liu, Hui Lei, Yue Shi, Jin-Ju Wang, Ning Chen, Zhang-Hua Li, Yang-Fang Chen, Qi-Fa Ye, Yi Yang
Overload-exercise (OE) causes myocardial injury through inducing autophagy and apoptosis. In this study we examined whether an autophagy inhibitor 3-methyladenine (3-MA) could alleviate OE-induced cardiac injury. Rats were injected with 3-MA (15 mg/kg, iv) or saline before subjected to various intensities of OE, including no swim (control), 2 h swim (mild-intensity exercise, MIE), 2 h swim with 2.5% body weight overload (moderate OE; MOE), 5% overload (intensive OE; IOE) or 2.5% overload until exhausted (exhaustive OE; EOE)...
March 6, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28243129/polydatin-regulates-proliferation-apoptosis-and-autophagy-in-multiple-myeloma-cells-through-mtor-p70s6k-pathway
#6
Baojun Yang, Shunxin Zhao
BACKGROUND: Polydatin (PD) plays an important role in suppressing platelet aggregation, reducing blood lipid, restoring microcirculation and protecting from myocardial ischemia/reperfusion injury and shock. In addition, PD possesses anticancer activity. However, the effect and the mechanism of PD in regulating multiple myeloma (MM) cell survival and death are still unknown. METHODS: Cell proliferation and apoptosis of RPMI 8226 cells, respectively, were analyzed by cell counting kit8 (CCK-8) assay and flow cytometry...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/28225086/uvrag-deficiency-exacerbates-doxorubicin-induced-cardiotoxicity
#7
Lin An, Xiao-Wen Hu, Shasha Zhang, Xiaowen Hu, Zongpei Song, Amber Naz, Zhenguo Zi, Jian Wu, Can Li, Yunzeng Zou, Lin He, Hongxin Zhu
Doxorubicin (DOX) is an effective chemotherapeutic drug in the treatment of various types of cancers. However, its clinical application has been largely limited by potential development of cardiotoxicity. Previously we have shown that ultra-violet radiation resistance-associated gene (UVRAG), an autophagy-related protein, is essential for the maintenance of autophagic flux in the heart under physiological conditions. Here, we sought to determine the role of UVRAG-mediated autophagy in DOX-induced cardiotoxicity...
February 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28216152/1-25-dihydroxyvitamin-d3-prevents-the-development-of-diabetic-cardiomyopathy-in-type-1-diabetic-rats-by-enhancing-autophagy-via-inhibiting-the-%C3%AE-catenin-tcf4-gsk-3%C3%AE-mtor-pathway
#8
Huili Wei, Hua Qu, Hang Wang, Baolan Ji, Yao Ding, Dan Liu, Yang Duan, Huimin Liang, Chuan Peng, Xiaoqiu Xiao, Huacong Deng
Diabetic cardiomyopathy (DCM) can increase the risk of heart failure and death in diabetic patients. However, no effective approaches are available to prevent its progression and development. Studies have shown that vitamin D is greatly implicated in cardiac hypertrophy and fibrosis, and there is a high prevalence of vitamin D deficiency in diabetic patients. In this study, we investigated whether 1,25-Dihydroxyvitamin-D3 (1,25D3) can improve DCM through a vitamin D receptor (VDR)-dependent mechanism associated with autophagy and the β-catenin/T-cell factor/lymphoid enhancer factor (TCF4)/glycogen synthase kinase-3β (GSK-3β)/mammalian target of rapamycin (mTOR) pathway...
February 17, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28215799/comprehensive-understanding-of-pm2-5-on-gene-and-microrna-expression-patterns-in-zebrafish-danio-rerio-model
#9
Junchao Duan, Yang Yu, Yang Li, Li Jing, Man Yang, Ji Wang, Yanbo Li, Xianqing Zhou, Mark R Miller, Zhiwei Sun
PM2.5 is a major public health concern and some severe diseases have been attributed to exposure to PM2.5. However, a comprehensive understanding of gene and microRNA expression patterns induced by PM2.5 is missing. The objective of this study was to evaluate the toxicity of PM2.5 via genome-wide transcriptional analysis in the model teleost fish, zebrafish (Danio rerio). Gene ontology analysis revealed that the most impact gene functional categories induced by PM2.5 included oxidation-reduction process, transport, response to xenobiotic stimulus, response to chemical stimulus and metabolic process...
May 15, 2017: Science of the Total Environment
https://www.readbyqxmd.com/read/28198521/sevoflurane-ameliorates-doxorubicin-induced-myocardial-injury-by-affecting-the-phosphorylation-states-of-proteins-in-pi3k-akt-mtor-signaling-pathway
#10
Yini Wu, Jianping Wang, Xiaoyan Yu, Dongli Li, Xin Han, Lihua Fan
BACKGROUND: The effect of sevoflurane on the doxorubicin-induced myocardial injury was explored by investigating the phosphorylation states of proteins in phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway. METHODS: Myocardial injury rat models were induced by doxorubicin and evenly assigned into five groups according to different treatment: Doxorubicin group (DG, 200-µL saline solution), sevoflurane group (SevG, inhaled with 2...
February 15, 2017: Cardiology Journal
https://www.readbyqxmd.com/read/28164169/adeno-associated-virus-serotype-9-driven-expression-of-bag3-improves-left-ventricular-function-in-murine-hearts-with-left-ventricular-dysfunction-secondary-to-a-myocardial-infarction
#11
Tijana Knezevic, Valerie D Myers, Feifei Su, JuFang Wang, Jianliang Song, Xue-Qian Zhang, Erhe Gao, Guofeng Gao, Madesh Muniswamy, Manish K Gupta, Jennifer Gordon, Kristen N Weiner, Joseph Rabinowitz, Frederick V Ramsey, Douglas G Tilley, Kamel Khalili, Joseph Y Cheung, Arthur M Feldman
OBJECTIVES: The present study was undertaken to test the hypothesis that gene delivery of BCL2-Associated Athanogene 3 (BAG3) to the heart of mice with left ventricular dysfunction secondary to a myocardial infarction could enhance cardiac performance. BACKGROUND: BAG3 is a 575 amino acid protein that has pleotropic functions in the cell including pro-autophagy and anti-apoptosis. Mutations in BAG3 have been associated with both skeletal muscle dysfunction and familial dilated cardiomyopathy and BAG3 levels are diminished in non-familial heart failure...
December 2016: JACC. Basic to Translational Science
https://www.readbyqxmd.com/read/28159361/enhanced-autophagy-by-exenatide-mitigates-doxorubicin-induced-cardiotoxicity
#12
Kyung Hye Lee, Haneul Cho, Sora Lee, Jong Shin Woo, Byung Hyun Cho, Jung Hee Kang, Yun-Mi Jeong, Xian Wu Cheng, Weon Kim
OBJECTIVES: Exenatide is a glucagon-like peptide-1 analogue that mitigates myocardial injury caused by ischemia-reperfusion injury via the survival signaling pathway. We hypothesized that exenatide would provide a protective effect in doxorubicin-induced cardiotoxicity. METHODS: H9c2 cardiomyocytes were pre-treated with exenatide followed by doxorubicin (DOX), and cell viability and intracellular reactive oxygen species (ROS) were subsequently measured. In order to determine the role of autophagy, we performed western blot as well as TUNEL and autophagosome staining...
January 27, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28151484/berbamine-postconditioning-protects-the-heart-from-ischemia-reperfusion-injury-through-modulation-of-autophagy
#13
Yanjun Zheng, Shanshan Gu, Xuxia Li, Jiliang Tan, Shenyan Liu, Yukun Jiang, Caimei Zhang, Ling Gao, Huang-Tian Yang
Pretreatment of berbamine protects the heart from ischemia/reperfusion (I/R) injury. However it is unknown whether it has cardioprotection when given at the onset of reperfusion (postconditioning (PoC)), a protocol with more clinical impact. Autophagy is upregulated in I/R myocardium and exacerbates cardiomyocyte death during reperfusion. However, it is unknown whether the autophagy during reperfusion is regulated by berbamine. Here we investigated whether berbamine PoC (BMPoC) protects the heart through regulation of autophagy by analyzing the effects of BMPoC on infarct size and/or cell death, functional recovery and autophagy in perfused rat hearts and isolated cardiomyocytes subjected to I/R...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28150462/tongxinluo-exerts-protective-effects-via-anti-apoptotic-and-pro-autophagic-mechanisms-by-activating-ampk-pathway-in-infarcted-rat-hearts
#14
Qing Li, Na Li, He-He Cui, Xia-Qiu Tian, Chen Jin, Gui-Hao Chen, Yue-Jin Yang
Tongxinluo (TXL) has been demonstrated to have a protective role during ischemia/reperfusion after acute myocardial infarction (AMI), but the long-term effects and the underlying mechanisms are still unknown. This study aimed to investigate whether TXL could have an effect on apoptosis or autophagy of cardiomyocytes through the AMP-activated protein kinase (AMPK) pathway. Male, Sprague-Dawley rats (n = 75) were randomly divided to sham, control, TXL (4 mg kg(-1)  d(-1) orally), compound C (intraperitoneal injection at 10 mg kg(-1)  d(-1) ), and TXL + compound C groups...
February 1, 2017: Experimental Physiology
https://www.readbyqxmd.com/read/28108421/tlr4-knockout-attenuated-high-fat-diet-induced-cardiac-dysfunction-via-nf-%C3%AE%C2%BAb-jnk-dependent-activation-of-autophagy
#15
Nan Hu, Yingmei Zhang
Obesity is commonly associated with a low grade systemic inflammation, which may contribute to the onset and development of myocardial remodeling and contractile dysfunction. Toll-like receptor 4 (TLR4) plays an important role in innate immunity and inflammation although its role in high fat diet-induced obesity cardiac dysfunction remains elusive. This study was designed to examine the effect of TLR4 ablation on high fat diet intake-induced cardiac anomalies, if any, and underlying mechanism(s) involved. Wild-type (WT) and TLR4 knockout mice were fed normal or high fat (60% calorie from fat) diet for 12weeks prior to assessment of mechanical and intracellular Ca(2+) properties...
January 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28079007/novel-therapies-targeting-cardioprotection-and-regeneration
#16
Valeria Garrido, Evelyn Mendoza-Torres, Jaime A Riquelme, Ariel Díaz, Marcela Pizarro, Mario Bustamante, Myra N Chavez, María Paz Ocaranza, Rosemarie Mellado, Ramon Corbalan, Miguel L Allende, Sergio Lavandero
Cardiovascular disease is the leading cause of death worldwide. The heart is susceptible to pathologies that impact the myocardium directly, such myocardial infarction and consequent heart failure, as well as conditions with indirect cardiac effects, such cancer treatment-related cardiotoxicity. As the contractile cells of the heart, cardiomyocytes are essential for normal cardiac function. Various stress stimuli may result in transient damage or cell death in cardiomyocytes through apoptosis, necrosis or maladaptive autophagy...
January 12, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28036273/nerve-growth-factor-induced-akt-mtor-activation-protects-the-ischemic-heart-via-restoring-autophagic-flux-and-attenuating-ubiquitinated-protein-accumulation
#17
Zhou-Guang Wang, Hao Li, Yan Huang, Rui Li, Xiao-Fan Wang, Li-Xia Yu, Xue-Qiang Guang, Lei Li, Hong-Yu Zhang, Ying-Zheng Zhao, Chunxiang Zhang, Xiao-Kun Li, Rong-Zhou Wu, Mao-Ping Chu, Jian Xiao
The dysregulation of autophagy is related to a variety of cardiovascular diseases, such as myocardial ischemia/reperfusion (I/R). Nerve growth factor (NGF) has been shown to have therapeutic potential in ischaemic heart injury. In this study, we demonstrate that NGF administration can accelerate autophagic flux and attenuate protein ubiquitination in myocardial I/R heart. Our results showed that NGF could restored heart function and decreased the apoptosis of cardiomyocytes which induced by myocardial I/R injury...
December 27, 2016: Oncotarget
https://www.readbyqxmd.com/read/28013216/diesel-exhaust-particles-contribute-to-endothelia-apoptosis-via-autophagy-pathway
#18
Jhih-Syuan Wang, Chia-Yi Tseng, Ming-Wei Chao
Epidemiological studies suggest that an increase of PM2.5 diesel exhaust particles (DEP) in ambient air corresponds to increased myocardial infarctions and atherosclerosis. When exposed to DEP, endothelial cells exhibit increases in oxidative stress and apoptosis, but the role of autophagy in this DEP-induced cell death remains unclear. Here, we suggest that acute DEP exposure produces intracellular ROS leading to induction of DEP internalization, endothelial dysfunction, and pro-inflammation in an in vitro HUVEC model...
December 24, 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/27998869/-role-of-autophagy-in-fasudil-induced-rho-kinase-inhibition-for-protection-against-myocardial-ischemia-reperfusion-injury-in-rats
#19
Hong-Wei Ye, Ting-Ting Fang, Xiao-Yu Gu, Ya Wang, Guang-Yu Zhu, Ying Yu, Qin Gao
OBJECTIVE: To investigate the changes of autophagy in ischemic myocardium of rats treated with fasudil for inhibiting Rho kinase. METHODS: The hearts isolated from male Sprague-Dawley rats were subjected to 30 min of occlusion of the left anterior descending artery followed by 120 min of reperfusion with or without treatment with fasudil or fasudil+Wort. The left ventricular hemodynamics were continuously recorded, and the coronary effluent was collected during the reperfusion to determine lactate dehydrogenase (LDH) levels...
December 20, 2016: Nan Fang Yi Ke da Xue Xue Bao, Journal of Southern Medical University
https://www.readbyqxmd.com/read/27994061/focal-adhesion-kinase-mediated-phosphorylation-of-beclin1-protein-suppresses-cardiomyocyte-autophagy-and-initiates-hypertrophic-growth
#20
Zhaokang Cheng, Qiang Zhu, Rachel Dee, Zachary Opheim, Christopher P Mack, Douglas M Cyr, Joan M Taylor
Autophagy is an evolutionarily conserved intracellular degradation/recycling system that is essential for cellular homeostasis but is dysregulated in a number of diseases, including myocardial hypertrophy. Although it is clear that limiting or accelerating autophagic flux can result in pathological cardiac remodeling, the physiological signaling pathways that fine-tune cardiac autophagy are poorly understood. Herein, we demonstrated that stimulation of cardiomyocytes with phenylephrine (PE), a well known hypertrophic agonist, suppresses autophagy and that activation of focal adhesion kinase (FAK) is necessary for PE-stimulated autophagy suppression and subsequent initiation of hypertrophic growth...
February 10, 2017: Journal of Biological Chemistry
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