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autophage myocardial infarction

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https://www.readbyqxmd.com/read/29665360/alpha7-nicotinic-acetylcholine-receptor-activation-protects-against-myocardial-reperfusion-injury-through-modulation-of-autophagy
#1
Zuoxu Hou, Yaguang Zhou, Hongyan Yang, Yan Liu, Xuechao Mao, Xinghua Qin, Xiaoliang Li, Xing Zhang, Yuanyuan Hu
Alpha7 nicotinic acetylcholine receptor (α7nAChR) activation alleviates myocardial ischemia/reperfusion (MI/R) injury. However, the underlying mechanisms remain unclear. Here, we investigated the role of autophagy in α7nAChR-mediated cardioprotection and the molecular mechanisms involved. Activating α7nAChR with PNU-282987 at the initiation of reperfusion reduced myocardial infarct size in MI/R rats. PNU-282987 treatment also significantly inhibited MI/R-induced myocardial autophagy dysfunction as evidenced by the reduction of LC3-II/LC3-I ratio, Beclin-1 and p62 abundance...
April 14, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29652546/ataxia-telangiectasia-mutated-kinase-deficiency-impairs-autophagic-response-early-during-myocardial-infarction
#2
Patsy R Thrasher, Stephanie L C Scofield, Suman Dalal, Claire C Crawford, Mahipal Singh, Krishna Singh
Ataxia-telangiectasia mutated kinase (ATM) is activated in response to DNA damage. We have previously shown that ATM plays a critical role in myocyte apoptosis and cardiac remodeling following myocardial infarction (MI). Here, we tested the hypothesis that ATM deficiency results in autophagic impairment in the heart early during MI. MI was induced in wild-type (WT) and ATM heterozygous knockout (hKO) mice by ligation of the left anterior descending artery (LAD). Structural and biochemical parameters of the heart were measured 4 hours following LAD ligation...
April 13, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29651246/lactone-component-from-ligusticum-chuanxiong-alleviates-myocardial-ischemia-injury-through-inhibiting-autophagy
#3
Gang Wang, Guoliang Dai, Jie Song, Maomao Zhu, Ying Liu, Xuefeng Hou, Zhongcheng Ke, Yuanli Zhou, Huihui Qiu, Fujing Wang, Nan Jiang, Xiaobin Jia, Liang Feng
The dysregulation of autophagy is associated with a series of cardiovascular diseases, such as myocardial ischemia injury. Lactone component from Ligusticum chuanxiong (LLC) is the major constituent of the traditional Chinese herb L. chuanxiong Hort., which has been reported to hold potential cardioprotective effects. In this study, to determine whether LLC protects the heart through regulation of autophagy, we explored the effects of LLC on cardioprotection and autophagy in myocardial ischemia injured rats and H9c2 cardiomyocytes...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29531824/nr4a2-protects-cardiomyocytes-against-myocardial-infarction-injury-by-promoting-autophagy
#4
Honghong Liu, Pingping Liu, Xingxing Shi, Deling Yin, Jing Zhao
Myocardial infarction (MI), characterized by ischemia-induced cardiomyocyte apoptosis, is the leading cause of mortality worldwide. NR4A2, a member of the NR4A orphan nucleus receptor family, is upregulated in mouse hearts with MI injury. Furthermore, NR4A2 knockdown aggravates heart injury as evidenced by enlarged hearts and increased apoptosis. To elucidate the underlying mechanisms of NR4A2-regulated apoptosis, we used H9c2 cardiomyocytes deprived of serum and neonatal rat cardiomyocytes (NRCMs) exposed to hypoxia to mimic ischemic conditions in vivo...
December 2018: Cell Death Discovery
https://www.readbyqxmd.com/read/29426003/programmed-necrosis-in-heart-disease-molecular-mechanisms-and-clinical-implications
#5
Hong Zhu, Aijun Sun
Programmed cell death plays an essential role in myocardial homeostasis and pathology. Three distinct forms of programmed cell death have been identified, namely apoptosis, necrosis, and autophagic cell death. Necrosis, previously known as an unregulated form of cell death, has been recognized as a highly regulated process now and attracted great attention over the past decade. Programmed necrosis mainly refers to necroptosis, pyroptosis, ferroptosis, and mitochondrial permeability transition (MPT)-dependent necrosis...
March 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29237156/potential-involvement-of-mir-30e-3p-in-myocardial-injury-induced-by-coronary-microembolization-via-autophagy-activation
#6
Xian-Tao Wang, Xiao-Dan Wu, Yuan-Xi Lu, Yu-Han Sun, Han-Hua Zhu, Jia-Bao Liang, Wen-Kai He, Zhi-Yu Zeng, Lang Li
BACKGROUND/AIMS: Coronary microembolization (CME) can lead to no-reflow or slow reflow, which is one of the important reasons for loss of clinical benefit from myocardial reperfusion therapy. MicroRNAs and autophagy are heavily implicated in the occurrence and development of almost all cardiovascular diseases. Therefore, the present study was designed to investigate the role of miR-30e-3p and autophagy in CME-induced myocardial injury rat model. METHODS: Sixty rats were randomly divided into six groups: sham, CME 1h,3h,6h,9h, and 12h (n = 10 per group)...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29127009/nicorandil-alleviates-myocardial-injury-and-post-infarction-cardiac-remodeling-by-inhibiting-mst1
#7
Shanjie Wang, Yanhong Fan, Xinyu Feng, Chuang Sun, Zhaofeng Shi, Tian Li, Jianjun Lv, Zhi Yang, Zhijing Zhao, Dongdong Sun
BACKGROUND: Cardiomyocyte autophagy and apoptosis are crucial events underlying the development of cardiac abnormalities and dysfunction after myocardial infarction (MI). A better understanding of the cell signaling pathways involved in cardiac remodeling may support the development of new therapeutic strategies for the treatment of heart failure (HF) after MI. METHODS: A cardiac MI injury model was constructed by ligating the left anterior descending (LAD) coronary artery...
January 1, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28945004/tlr3-contributes-to-persistent-autophagy-and-heart-failure-in-mice-after-myocardial-infarction
#8
Ting Gao, Shao-Ping Zhang, Jian-Fei Wang, Li Liu, Yin Wang, Zhi-Yong Cao, Qi-Kuan Hu, Wen-Jun Yuan, Li Lin
Toll-like receptors (TLRs) are essential immunoreceptors involved in host defence against invading microbes. Recent studies indicate that certain TLRs activate immunological autophagy to eliminate microbes. It remains unknown whether TLRs regulate autophagy to play a role in the heart. This study examined this question. The activation of TLR3 in cultured cardiomyocytes was observed to increase protein levels of autophagic components, including LC3-II, a specific marker for autophagy induction, and p62/SQSTM1, an autophagy receptor normally degraded in the final step of autophagy...
January 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28942152/relaxin-alleviates-tgf%C3%AE-1-induced-cardiac-fibrosis-via-inhibition-of-stat3-dependent-autophagy
#9
Yue Yuan, Yun Zhang, Xuejie Han, Yanyan Li, Xinbo Zhao, Li Sheng, Yue Li
Cardiac fibrosis is a pathological feature common to a variety of heart diseases such as myocardial infarction, arrhythmias, cardiomyopathies and heart failure. Emerging data has indicted that autophagy is involved in fibrotic synthesis. Relaxin as a pleiotropic hormone can attenuate cardiac fibrosis and hypertrophy, however the exact molecular mechanism remains largely unknown. In this work, we evaluated whether the antifibrotic effect of relaxin relies on regulating autophagy in primary cardiac fibroblasts (CFs)...
December 2, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28825851/restoring-diabetes-induced-autophagic-flux-arrest-in-ischemic-reperfused-heart-by-adipor-adiponectin-receptor-activation-involves-both-ampk-dependent-and-ampk-independent-signaling
#10
Yajing Wang, Bin Liang, Wayne Bond Lau, Yunhui Du, Rui Guo, Zheyi Yan, Lu Gan, Wenjun Yan, Jianli Zhao, Erhe Gao, Walter Koch, Xin-Liang Ma
Macroautophagy/autophagy is increasingly recognized as an important regulator of myocardial ischemia-reperfusion (MI-R) injury. However, whether and how diabetes may alter autophagy in response to MI-R remains unknown. Deficiency of ADIPOQ, a cardioprotective molecule, markedly increases MI-R injury. However, the role of diabetic hypoadiponectinemia in cardiac autophagy alteration after MI-R is unclear. Utilizing normal control (NC), high-fat-diet-induced diabetes, and Adipoq knockout (adipoq-/- ) mice, we demonstrated that autophagosome formation was modestly inhibited and autophagosome clearance was markedly impaired in the diabetic heart subjected to MI-R...
2017: Autophagy
https://www.readbyqxmd.com/read/28694354/myocardial-upregulation-of-cathepsin-d-by-ischemic-heart-disease-promotes-autophagic-flux-and-protects-against-cardiac-remodeling-and-heart-failure
#11
Penglong Wu, Xun Yuan, Faqian Li, Jianhua Zhang, Wei Zhu, Meng Wei, Jingbo Li, Xuejun Wang
BACKGROUND: Lysosomal dysfunction is implicated in human heart failure for which ischemic heart disease is the leading cause. Altered myocardial expression of CTSD (cathepsin D), a major lysosomal protease, was observed in human heart failure, but its pathophysiological significance has not been determined. METHODS AND RESULTS: Western blot analyses revealed an increase in the precursor but not the mature form of CTSD in myocardial samples from explanted human failing hearts with ischemic heart disease, which is recapitulated in chronic myocardial infarction produced via coronary artery ligation in Ctsd(+/+) but not Ctsd(+/-) mice...
July 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/28598232/exercise-reestablishes-autophagic-flux-and-mitochondrial-quality-control-in-heart-failure
#12
Juliane C Campos, Bruno B Queliconi, Luiz H M Bozi, Luiz R G Bechara, Paulo M M Dourado, Allen M Andres, Paulo R Jannig, Kátia M S Gomes, Vanessa O Zambelli, Cibele Rocha-Resende, Silvia Guatimosim, Patricia C Brum, Daria Mochly-Rosen, Roberta A Gottlieb, Alicia J Kowaltowski, Julio C B Ferreira
We previously reported that facilitating the clearance of damaged mitochondria through macroautophagy/autophagy protects against acute myocardial infarction. Here we characterize the impact of exercise, a safe strategy against cardiovascular disease, on cardiac autophagy and its contribution to mitochondrial quality control, bioenergetics and oxidative damage in a post-myocardial infarction-induced heart failure animal model. We found that failing hearts displayed reduced autophagic flux depicted by accumulation of autophagy-related markers and loss of responsiveness to chloroquine treatment at 4 and 12 wk after myocardial infarction...
August 3, 2017: Autophagy
https://www.readbyqxmd.com/read/28546358/autophagy-and-mitophagy-in-cardiovascular-disease
#13
REVIEW
José Manuel Bravo-San Pedro, Guido Kroemer, Lorenzo Galluzzi
Autophagy contributes to the maintenance of intracellular homeostasis in most cells of cardiovascular origin, including cardiomyocytes, endothelial cells, and arterial smooth muscle cells. Mitophagy is an autophagic response that specifically targets damaged, and hence potentially cytotoxic, mitochondria. As these organelles occupy a critical position in the bioenergetics of the cardiovascular system, mitophagy is particularly important for cardiovascular homeostasis in health and disease. Consistent with this notion, genetic defects in autophagy or mitophagy have been shown to exacerbate the propensity of laboratory animals to spontaneously develop cardiodegenerative disorders...
May 26, 2017: Circulation Research
https://www.readbyqxmd.com/read/28420993/phellinus-linteus-mycelium-alleviates-myocardial-ischemia-reperfusion-injury-through-autophagic-regulation
#14
Hsing-Hui Su, Ya-Chun Chu, Jiuan-Miaw Liao, Yi-Hsin Wang, Ming-Shiou Jan, Chia-Wei Lin, Chiu-Yeh Wu, Chin-Yin Tseng, Jiin-Cherng Yen, Shiang-Suo Huang
The incidence of myocardial ischemia-reperfusion (IR) injury is rapidly increasing around the world and this disease is a major contributor to global morbidity and mortality. It is known that regulation of programmed cell death including apoptosis and autophagy reduces the impact of myocardial IR injury. In this study, the cardioprotective effects and underlying mechanisms of Phellinus linteus (Berk. and Curt.) Teng, Hymenochaetaceae (PL), a type of medicinal mushroom, were examined in rats subjected to myocardial IR injury...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28287478/myocardial-ischemic-postconditioning-promotes-autophagy-against-ischemia-reperfusion-injury-via-the-activation-of-the-nnos-ampk-mtor-pathway
#15
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/28151484/berbamine-postconditioning-protects-the-heart-from-ischemia-reperfusion-injury-through-modulation-of-autophagy
#16
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
#17
Qing Li, Na Li, He-He Cui, Xia-Qiu Tian, Chen Jin, Gui-Hao Chen, Yue-Jin Yang
What is the central question of this study? In a rat model of acute myocardial infarction (AMI), we investigated the effect of Tongxinluo (TXL) treatment. Does TXL activate autophagy and attenuate apoptosis of cardiomyocytes through the AMPK pathway to facilitate survival of cardiomyocytes and improve cardiac function? What is the main finding and its importance? Major findings are as follows: (i) TXL treatment preserved cardiac function and reduced ventricular remodelling, infarct size and inflammation in rat hearts after AMI; (ii) TXL treatment dramatically increased autophagy and inhibited apoptosis in myocardium; and (iii) the AMPK signalling pathway played a crucial role in mediating the beneficial effects of TXL...
April 1, 2017: Experimental Physiology
https://www.readbyqxmd.com/read/27857190/simulated-ischemia-reperfusion-induced-p65-beclin-1-dependent-autophagic-cell-death-in-human-umbilical-vein-endothelial-cells
#18
Min Zeng, Xin Wei, Zhiyong Wu, Wei Li, Yin Zheng, Bing Li, Xuqing Meng, Xiuhong Fu, Yi Fei
Myocardial ischemia/reperfusion (I/R) injury detrimentally alters the prognosis of patients undergoing revascularization after acute myocardial infarction. Our previous study demonstrated that NF-κB-induced autophagy plays a detrimental role in cardiac I/R injury using a rabbit myocardial I/R model. In this study, we sought to explore the specific mechanism of this autophagy-mediated cell damage in an in vitro simulated ischemia/reperfusion (sI/R) model using human umbilical vein endothelial cells. Our current study demonstrates that simulated I/R induces autophagy in a p65-Beclin 1-dependent manner, which can be suppressed with the inhibition of NF-κB...
November 18, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27830000/ampk-mediated-cardioprotection-of-atorvastatin-relates-to-the-reduction-of-apoptosis-and-activation-of-autophagy-in-infarcted-rat-hearts
#19
Qing Li, Qiu-Ting Dong, Yue-Jin Yang, Xia-Qiu Tian, Chen Jin, Pei-Sen Huang, Lei-Pei Jiang, Gui-Hao Chen
Atorvastatin (ATV) has an important pro-survival role in cardiomyocytes after acute myocardial infarction (AMI). The objectives of this study were to: 1) determine whether ATV could affect autophagy of cardiomyocytes via the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway, and 2) investigate the balance between autophagy and apoptosis pathways. Male Wistar rats (n = 100) were randomly divided into sham, control, ATV, Compound C, and ATV+ Compound C groups. In this AMI model, drug treatments were administered for 1 week before induction of MI by surgical ligation, and measurements were taken 1 and 4 weeks after AMI induction...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27825852/osm-mitigates-post-infarction-cardiac-remodeling-and-dysfunction-by-up-regulating-autophagy-through-mst1-suppression
#20
Jianqiang Hu, Lei Zhang, Zhijing Zhao, Mingming Zhang, Jie Lin, Jiaxing Wang, Wenjun Yu, Wanrong Man, Congye Li, Rongqing Zhang, Erhe Gao, Haichang Wang, Dongdong Sun
The incidence and prevalence of heart failure (HF) in the world are rapidly rising possibly attributed to the worsened HF following myocardial infarction (MI) in recent years. Here we examined the effects of oncostatin M (OSM) on postinfarction cardiac remodeling and the underlying mechanisms involved. MI model was induced using left anterior descending coronary artery (LAD) ligation. In addition, cultured neonatal mouse cardiomyocytes were subjected to simulated MI. Our results revealed that OSM alleviated left ventricular remodeling, promoted cardiac function, restored mitochondrial cristae density and architecture disorders after 4weeks of MI...
August 2017: Biochimica et Biophysica Acta
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