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autophagy ischemia

Yang Yuan, Shan-Shan Pan
BACKGROUND: Late exercise preconditioning (LEP) is confirmed to have a protective effect on acute cardiovascular stress. However, the mechanisms by which mitophagy participates in EP-induced cardioprotection remain unclear. LEP may involve mitophagy mediated by the receptors PARK2 gene-encoded E3 ubiquitin ligase (Parkin) and BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (Bnip3) to scavenge damaged mitochondria. METHODS: Our exercise preconditioning (EP) protocol involved four 10-minute periods of running, separated by 10-minute recovery intervals, plus a period of exhaustive running at 24 hours after EP...
March 9, 2018: Journal of Cardiovascular Pharmacology
Pengzhou Hang, Jing Zhao, Zhenli Su, Hanqi Sun, Tingting Chen, Lihui Zhao, Zhimin Du
Backgroud/Aims: Growing evidence suggests that both cardiomyocyte apoptosis and excessive autophagy exacerbates cardiac dysfunction during myocardial ischemia-reperfusion (IR). As a precursor of acetylcholine, choline has been found to protect the heart by repressing ischemic cardiomyocyte apoptosis. However, the relationship between choline and cardiomyocyte autophagy is unclear. The present study aimed to investigate whether autophagy was involved in the cardioprotection of choline during IR. METHODS: Rats were subjected to 30 min reversible ischemia by ligation of left anterior descending coronary artery followed by reperfusion for 2 h...
March 7, 2018: Cellular Physiology and Biochemistry
Jianjie Zheng, Jing Li, Bo Kou, Qiuyue Yi, Tao Shi
The aim of the present study was to determine the cardioprotective mechanisms by which micro (mi)RNA-30e protects the heart from myocardial ischemia/reperfusion injury (MI/R) and to explore the signaling pathways that may confer protection for the heart and be potential therapeutic targets. It was demonstrated that miRNA‑30e expression was decreased in patients with MI/R. In H9C2 cells, silencing (si)miRNA‑30e significantly inhibited cellular apoptosis, the expression of apoptosis regulator BAX (Bax) and caspase‑3 activity...
March 7, 2018: International Journal of Molecular Medicine
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
Ying Liu, HongNa Yang, GuoYong Jia, Lan Li, Hui Chen, JianZhong Bi, CuiLan Wang
BACKGROUND: It is well accepted that both rosuvastatin and resveratrol exert neuroprotective effects on cerebral ischemia/reperfusion injury through some common pathways. Resveratrol has also been demonstrated to protect against cerebral ischemia/reperfusion injury through enhancing autophagy. Thus, we hypothesized that combined rosuvastatin and resveratrol pretreatment had synergistic effects on cerebral ischemia/reperfusion injury. MATERIALS AND METHODS: Adult male Sprague Dawley rats receiving middle cerebral artery occlusion surgery as animal model of cerebral ischemia/reperfusion injury were randomly assigned to 4 groups: control, resveratrol alone pretreatment, rosuvastatin alone pretreatment, and combined rosuvastatin and resveratrol pretreatment...
March 7, 2018: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
Tian Li, Yafeng Shen, Li Su, Xiaoyan Fan, Fangxing Lin, Xuting Ye, Dianer Ding, Ying Tang, Yang Yongji, Changhai Lei, Shi Hu
Post-ischemic heart failure is a major cause of death worldwide. Reperfusion of infarcted heart tissue after myocardial infarction has been an important medical intervention to improve outcomes. However, disturbances in Ca2+ and redox homeostasis at the cellular level caused by ischemia/reperfusion remain major clinical challenges. In this study, we investigated the potential of adeno-associated virus (AAV)-9-mediated cardiac expression of a Type-2 ryanodine receptor (RyR2) degradation-associated gene, Presenilin 1 (PSEN1), to combat post-ischemic heart failure...
March 9, 2018: Journal of Drug Targeting
Emine Sekerdag, Ihsan Solaroglu, Yasemin Gursoy-Ozdemir
As a result of ischemia or hemorrhage, blood supply to neurons is disrupted which subsequently promotes a cascade of pathophysiological responses resulting in cell loss. Many mechanisms are involved solely or in combination in this disorder including excitotoxicity, mitochondrial death pathways, and the release of free radicals, protein misfolding, apoptosis, necrosis, autophagy and inflammation. Besides neuronal cell loss, damage to and loss of astrocytes as well as injury to white matter contributes also to cerebral injury...
March 1, 2018: Current Neuropharmacology
Yanyan Zhang, Yuan Zhang, Jiayu Tang, Shuang Zhao, Chen Li, Yong-Pan Huang, Minhan Yi
BACKGROUND/AIMS: Genetic or nutritional deficiencies in homocysteine (Hcy)metabolism lead to the accumulation of Hcy and its metabolites in the blood. This can lead to hyperhomocysteinemia (HHcy), which is an independent risk factor for cardiovascular disease. Studies have shown that HHcy leads to endothelial dysfunction, a hallmark of atherosclerosis, which may explain this link. The precise mechanism remains unclear, but a strong possibility is excessive HHCy-induced autophagy. Autophagy has been better studied in ischemia/reperfusion (I/R) injuries, and previous work showed that Oxymatrine (OMT), a quinolizidine alkaloid, protects cells against myocardial I/R injury by inhibiting autophagy...
February 28, 2018: Cellular Physiology and Biochemistry
Maria J Perez-Alvarez, Mario Villa Gonzalez, Irene Benito-Cuesta, Francisco G Wandosell
Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to develop effective pharmacological treatments. However, the underlying molecular mechanisms are complex and not completely understood. One of the main problems is the fact that the ischemic damage is time-dependent and ranges from negligible to massive, involving different cell types such as neurons, astrocytes, microglia, endothelial cells, and some blood-derived cells (neutrophils, lymphocytes, etc...
2018: Frontiers in Neuroscience
Ying Xie, Daofang Jiang, Jing Xiao, Chensheng Fu, Zhenxing Zhang, Zhibin Ye, Xiaoli Zhang
Ischemic preconditioning (IPC) has a strong renoprotective effect during renal ischemia/reperfusion (I/R) injury that is thought to relate to autophagy. However, the role of autophagy during IPC-afforded renoprotection and the precise mechanisms involved are unknown. In this study, an in vitro hypoxia/reoxygenation (H/R) model was established in which oxygen and glucose deprivation (OGD) was applied to renal cells for 15 h followed by reoxygenation under normal conditions for 30 min, 2 h or 6 h; transient OGD and subsequent reoxygenation were implemented before prolonged H/R injury to achieve hypoxic preconditioning (HPC)...
March 1, 2018: Cell Death & Disease
Bjorn T Tam, Angus P Yu, Eric W Tam, Douglas A Monks, Xu P Wang, Xiao M Pei, Su P Koh, Thomas K Sin, Helen K W Law, Felix N Ugwu, Rashmi Supriya, Benjamin Y Yung, Shea P Yip, S C Wong, Lawrence W Chan, Christopher W Lai, Pin Ouyang, Parco M Siu
Pressure-induced injury (PI), such as a pressure ulcer, in patients with limited mobility is a healthcare issue worldwide. PI is an injury to skin and its underlying tissue such as skeletal muscle. Muscle compression, composed of mechanical deformation of muscle and external load, leads to localized ischemia and subsequent unloading reperfusion and, hence, a pressure ulcer in bed-bound patients. Although the gross factors involved in PI have been identified, little is known about the exact disease mechanism or its links to apoptosis, autophagy and inflammation...
February 27, 2018: Scientific Reports
Jun Gu, Yu-Qi Fan, Hui-Li Zhang, Jian-An Pan, Jian-Ying Yu, Jun-Feng Zhang, Chang-Qian Wang
The clinical use of doxorubicin (DOX) is limited by cardiotoxicity, involving the dysregulation of autophagy and apoptosis in the myocardium, which were partly reversed by resveratrol (RSV) supplement. However, a definitive mechanisms accounting for DOX's cardiotoxicity and the protective role of RSV remain poorly defined. The aim of the present study was to clarify the specific role of E2F transcription factor 1(E2F1) in regulating autophagy and apoptosis in DOX-induced cardiotoxicity as well as the protective effects of RSV...
February 20, 2018: Biochemical Pharmacology
Meiling Wu, Huadan Zhang, Jiejing Kai, Feng Zhu, Jingyin Dong, Ziwei Xu, Michael Wong, Ling-Hui Zeng
Objective: Whether activation or inhibition of the mTOR pathway is beneficial to ischemic injury remains controversial. It may result from the different reaction of ischemic penumbra and core to modulation of mTOR pathway after cerebral ischemia-reperfusion injury in rats. Methods: Longa's middle cerebral artery occlusion (MCAO) method was conducted to induce the focal cerebral ischemia-reperfusion. Western blot analysis was used to examine the protein expression involving mTOR pathway, apoptosis, and autophagy-related proteins...
February 2018: Annals of Clinical and Translational Neurology
Hui-Rong Jing, Fu-Wen Luo, Xing-Ming Liu, Xiao-Feng Tian, Yun Zhou
AIM: To evaluate whether fish oil (FO) can protect liver injury induced by intestinal ischemia/reperfusion (I/R) via the AMPK/SIRT-1/autophagy pathway. METHODS: Ischemia in Wistar rats was induced by superior mesenteric artery occlusion for 60 min and reperfusion for 240 min. One milliliter per day of FO emulsion or normal saline was administered by intraperitoneal injection for 5 consecutive days to each animal. Animals were sacrificed at the end of reperfusion...
February 21, 2018: World Journal of Gastroenterology: WJG
Yanbo Fan, Haocheng Lu, Wenying Liang, Minerva T Garcia-Barrio, Yanhong Guo, Ji Zhang, Tianqing Zhu, Yibai Hao, Jifeng Zhang, Y E Chen
<u>Rationale:</u> Post-ischemic angiogenesis is critical to limit the ischemic tissue damage and improve the blood flow recovery. The regulation and the underlying molecular mechanisms of post-ischemic angiogenesis are not fully unraveled. Transcription factor-EB (TFEB) is emerging as a master gene for autophagy and lysosome biogenesis. However, the role of TFEB in vascular disease is less understood. <u>Objective:</u> We aimed to determine the role of endothelial TFEB in post-ischemic angiogenesis and its underlying molecular mechanism...
February 21, 2018: Circulation Research
Daric J Wible, Shawn B Bratton
Reactive oxygen species (ROS) are important signaling molecules that mediate oxidative stress and cellular damage when improperly regulated. ROS and oxidative stress can activate autophagy, which generally serves as a cytoprotective negative feedback mechanism to selectively eliminate sources of ROS, including mitochondria and peroxisomes. In this review we describe the mechanisms by which ROS directly and indirectly activate autophagy, and conversely, how selective autophagy suppresses the formation of ROS...
February 2018: Current Opinion in Toxicology
Hao Guo, Lei Zhao, Bodong Wang, Xia Li, Hao Bai, Haixiao Liu, Liang Yue, Wei Guo, Zhenyuan Bian, Li Gao, Dayun Feng, Yan Qu
Remote limb ischemic postconditioning (RIPoC) is a promising adjunct treatment for cerebral ischemia-reperfusion (IR) injury. However, the underlying mechanisms have not been fully elucidated yet. The present study aims to investigate potential involvement and regulatory mechanisms of autophagy in RIPoC treatment against cerebral IR injury in mice. Mice were subjected to 2 h middle cerebral artery occlusion (MCAO) then treated with vehicle, 3-methyladenine (3-MA, an autophagy inhibitor), or compound C (an AMPK inhibitor) at the onset of reperfusion...
February 13, 2018: Brain Research Bulletin
Zhen Zheng, Li Zhang, Yi Qu, Guoguang Xiao, Shiping Li, Shan Bao, Q Richard Lu, Dezhi Mu
Hypoxic-ischemic encephalopathy (HIE) is a serious disease for neonates. However, present therapeutic strategies are not effective enough for treating HIE. Previous study showed that mesenchymal stem cells (MSCs) can exert neuroprotective effects for brain damage, but its mechanism remains elusive. Using in vitro coculture of rat cortical primary neurons and MSCs in HI conditions, we demonstrated that MSCs help increase brain derived neurotrophic factor (BDNF) and autophagy markers (LC3II and Beclin1) in the cultures and decrease cells death (lactate dehydrogenase levels)...
February 16, 2018: Stem Cells
Zhao Lei, Meihong Deng, Zhongjie Yi, Qian Sun, Richard A Shapiro, Hongbo Xu, Tunliang Li, Patricia A Loughran, John E Griepentrog, Hai Huang, Melanie J Scott, Feizhou Huang, Timothy R Billiar
Liver ischemia/reperfusion (I/R) injury occurs through induction of oxidative stress and release of damage-associated molecular patterns (DAMPs), including cytosolic DNA released from dysfunctional mitochondria or from the nucleus. Cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) is a cytosolic DNA sensor known to trigger stimulator of interferon genes (STING) and downstream type1 interferon (IFN-I) pathways, which are pivotal innate immune system responses to pathogen. However, little is known about the role of cGAS/STING in liver I/R injury...
February 15, 2018: American Journal of Physiology. Gastrointestinal and Liver Physiology
Niraj Kumar Jha, Saurabh Kumar Jha, Renu Sharma, Dhiraj Kumar, Rashmi K Ambasta, Pravir Kumar
For the maintenance of cellular homeostasis and energy metabolism, an uninterrupted supply of oxygen (O2) is routinely required in the brain. However, under the impaired level of O2 (hypoxia) or reduced blood flow (ischemia), the tissues are not sufficiently oxygenated, which triggers disruption of cellular homeostasis in the brain. Hypoxia is known to have a notable effect on controlling the expression of proteins involved in a broad range of biological processes varying from energy metabolism, erythropoiesis, angiogenesis, neurogenesis to mitochondrial trafficking and autophagy, thus facilitating neuronal cells to endure in deprived O2...
2018: Journal of Alzheimer's Disease: JAD
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