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autophage myocardial infarction

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https://www.readbyqxmd.com/read/29880830/histamine-deficiency-aggravates-cardiac-injury-through-mir-206-216b-atg13-axis-mediated-autophagic-dependant-apoptosis
#1
Suling Ding, Mieradilijiang Abudupataer, Zheliang Zhou, Jinmiao Chen, Hui Li, Lili Xu, Weiwei Zhang, Shuning Zhang, Yunzeng Zou, Tao Hong, Timothy C Wang, Xiangdong Yang, Junbo Ge
Histamine is a widely distributed biogenic amine involved in the regulation of an array of biological processes. Serum histamine level is markedly elevated in the early stages of acute myocardial infarction, whereas the role it plays remains unclear. Histidine decarboxylase (HDC) is the unique enzyme responsible for histamine production, and cardiac injury is significantly aggravated in HDC knockout mice (HDC-/- ), in which histamine is deficient. We also observed that autophagy was highly activated in cardiomyocytes of HDC-/- mice post acute myocardial infarction (AMI), which was abolished by compensation of exogenous histamine...
June 7, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29872406/tongguan-capsule-mitigates-post-myocardial-infarction-remodeling-by-promoting-autophagy-and-inhibiting-apoptosis-role-of-sirt1
#2
Shuai Mao, Peipei Chen, Ting Li, Liheng Guo, Minzhou Zhang
Left ventricular (LV) adverse remodeling and the concomitant functional deterioration contributes to the poor prognosis of patients with myocardial infarction (MI). Thus, a more effective treatment strategy is needed. Tongguan capsule (TGC), a patented Chinese medicine, has been shown to be cardioprotective in both humans and animals following ischemic injury, although its precise mechanism remains unclear. To investigate whether TGC can improve cardiac remodeling in the post-infarct heart, adult C57/BL6 mice underwent coronary artery ligation and were administered TGC or vehicle (saline) for 6 weeks...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29737434/anti-apoptosis-in-nonmyocytes-and-pro-autophagy-in-cardiomyocytes-two-strategies-against-postinfarction-heart-failure-through-regulation-of-cell-death-degeneration
#3
REVIEW
Genzou Takemura, Hiromitsu Kanamori, Hideshi Okada, Nagisa Miyazaki, Takatomo Watanabe, Akiko Tsujimoto, Kazuko Goto, Rumi Maruyama, Takako Fujiwara, Hisayoshi Fujiwara
Anti-apoptotic therapy for cardiomyocytes could be an effective strategy for preventing or treating heart failure. Notably, however, morphological evidence definitively demonstrating cardiomyocyte apoptosis has been very rare in actual heart diseases such as acute myocardial infarction and heart failure. By contrast, within the postinfarction heart, interstitial noncardiomyocytes such as granulation tissue cells do die via apoptosis to form scar tissue. Blockade of this apoptosis improves survival and mitigates ventricular remodeling and dysfunction during the chronic stage...
May 8, 2018: Heart Failure Reviews
https://www.readbyqxmd.com/read/29730286/vaspin-alleviates-myocardial-ischaemia-reperfusion-injury-via-activating-autophagic-flux-and-restoring-lysosomal-function
#4
Feihong Yang, Li Xue, Ziqi Han, Feng Xu, Shengchuan Cao, Shuai Dai, Baoshan Liu, Qiuhuan Yuan, Zheng Wang, Ping Guo, Yuguo Chen
Visceral adipose tissue-derived serine protease inhibitor (vaspin), as a secretory adipokine, was reported to exert a protective role on insulin resistance. Recent studies showed that serum vaspin level was downregulated in patients with coronary artery disease. However, whether vaspin exerted specific effects on myocardial injury remains unknown. In this study, we determined to explore the role of vaspin overexpression in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. Our results showed that the systemic delivery of adeno-associated virus-vaspin to mice reduced myocardial infarct size and apoptosis, and improved cardiac function after reperfusion, accompanied with upregulated autophagic flux and restored lysosomal function in the ischaemic heart...
May 3, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29680826/inflammation-autophagy-and-apoptosis-after-myocardial-infarction
#5
Xianwei Wang, Zhikun Guo, Zufeng Ding, Jawahar L Mehta
BACKGROUND: There is evidence for inflammation, autophagy, and apoptosis in the ischemic heart. Autophagy is a physiologic process for tissue survival. Apoptosis, on the other hand, is a mechanism that serves to clear the debris in the setting of tissue injury. The balance between autophagy and apoptosis may be important in cell survival and cardiac function. METHODS AND RESULTS: We examined the interplay of inflammation and myocyte autophagy and apoptosis during the ischemic process...
April 21, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29665360/alpha7-nicotinic-acetylcholine-receptor-activation-protects-against-myocardial-reperfusion-injury-through-modulation-of-autophagy
#6
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...
June 2, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29652546/ataxia-telangiectasia-mutated-kinase-deficiency-impairs-autophagic-response-early-during-myocardial-infarction
#7
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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
#15
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
#16
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
#17
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
#18
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
#19
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
#20
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
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