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Cardiac autophagy

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https://www.readbyqxmd.com/read/29895585/metformin-improves-neurologic-outcome-via-amp-activated-protein-kinase-mediated-autophagy-activation-in-a-rat-model-of-cardiac-arrest-and-resuscitation
#1
Juan Zhu, Kewei Liu, Kaibin Huang, Yong Gu, Yafang Hu, Suyue Pan, Zhong Ji
BACKGROUND: Sudden cardiac arrest (CA) often results in severe injury to the brain, and neuroprotection after CA has proved to be difficult to achieve. Herein, we sought to investigate the effects of metformin pretreatment on brain injury secondary to CA and cardiopulmonary resuscitation. METHODS AND RESULTS: Rats were subjected to 9-minute asphyxial CA after receiving daily metformin treatment for 2 weeks. Survival rate, neurologic deficit scores, neuronal loss, AMP-activated protein kinase (AMPK), and autophagy activation were assessed at indicated time points within the first 7 days after return of spontaneous circulation...
June 12, 2018: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29894736/torpor-arousal-cycles-in-syrian-hamster-heart-are-associated-with-transient-activation-of-the-protein-quality-control-system
#2
Marit Wiersma, Thais M A Beuren, Edwin L de Vrij, Vera A Reitsema, Jantje J Bruintjes, Hjalmar R Bouma, Bianca J J M Brundel, Robert H Henning
Hibernation consists of torpor, with marked suppression of metabolism and physiological functions, alternated with arousal periods featuring their full restoration. The heart is particularly challenged, exemplified by its rate reduction from 400 to 5-10 beats per minute during torpor in Syrian hamsters. In addition, during arousals, the heart needs to accommodate the very rapid return to normal function, which lead to our hypothesis that cardiac function during hibernation is supported by maintenance of protein homeostasis through adaptations in the protein quality control (PQC) system...
June 9, 2018: Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology
https://www.readbyqxmd.com/read/29887448/pten-induced-putative-kinase-1-pink1-alleviates-angiotensin-ii-induced-cardiac-injury-by-ameliorating-mitochondrial-dysfunction
#3
Wenjun Xiong, Jinghai Hua, Zuheng Liu, Wanqiang Cai, Yujia Bai, Qiong Zhan, Wenyan Lai, Qingchun Zeng, Hao Ren, Dingli Xu
BACKGROUND: Mitochondrial quality control is crucial to the development of angiotensin II (AngII)-induced cardiac hypertrophy. PTEN induced putative kinase 1 (PINK1) is rapidly degraded in normal mitochondria but accumulates in damaged mitochondria, triggering autophagy to protect cells. PINK1 mediates mitophagy in general, but whether PINK1 mediates AngII-induced mitophagy and the effects of PINK1 on AngII-induced injury are unknown. This study was designed to investigate the function of PINK1 in an AngII stimulation model and its regulation of AngII-induced mitophagy...
September 1, 2018: International Journal of Cardiology
https://www.readbyqxmd.com/read/29880830/histamine-deficiency-aggravates-cardiac-injury-through-mir-206-216b-atg13-axis-mediated-autophagic-dependant-apoptosis
#4
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/29879878/pure-polyphenols-applications-for-cardiac-health-and-disease
#5
Claudia N Santos, Andreia Gomes, Carole Oudot, Daniela Dias-Pedroso, Ana Rodriguez-Mateos, Helena L A Vieira, Catherine Brenner
Polyphenols are natural compounds present in fruits and vegetables that can exert beneficial effects on human health and notably, on the cardiovascular system. Some of these compounds showed significant protective activities toward atherosclerosis, hypertension, myocardial infarction, anthracyclin-induced cardiomyopathy, angiogenesis as well as heart failure. Polyphenols can act through systemic effects as well as through modulation of signaling pathways such as redox signaling, inflammation, autophagy and cell death in the heart and vessels...
June 7, 2018: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/29877162/experimental-spinal-cord-injury-causes-left-ventricular-atrophy-and-is-associated-with-an-upregulation-of-proteolytic-pathways
#6
Malihe-Sadat Poormasjedi-Meibod, Maral Mansouri, Mary Fossey, Jordan W Squair, Jie Liu, John H McNeill, Christopher R West
Spinal cord injury (SCI) causes autonomic dysfunction, altered neurohumoral control, profound hemodynamic changes, and an increased risk of heart disease. In this prospective study we investigated the cardiac consequences of chronic experimental SCI in rats by combining cutting edge in vivo techniques (magnetic resonance imaging (MRI) and left-ventricular (LV) pressure-volume catheterization) with histological and molecular assessments. 12 weeks post-SCI, MRI-derived structural indices and in vivo LV catheterization derived functional indices indicated the presence of LV atrophy (LV mass in Control vs...
June 7, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29875683/beneficial-autophagic-activities-mitochondrial-function-and-metabolic-phenotype-adaptations-promoted-by-high-intensity-interval-training-in-a-rat-model
#7
Fang-Hui Li, Tao Li, Jing-Yi Ai, Lei Sun, Zhu Min, Rui Duan, Ling Zhu, Yan-Ying Liu, Timon Cheng-Yi Liu
The effects of high-intensity interval (HIIT) and moderate-intensity continuous training (MICT) on basal autophagy and mitochondrial function in cardiac and skeletal muscle and plasma metabolic phenotypes have not been clearly characterized. Here, we investigated how 10-weeks HIIT and MICT differentially modify basal autophagy and mitochondrial markers in cardiac and skeletal muscle and conducted an untargeted metabolomics study with proton nuclear magnetic resonance (1 H NMR) spectroscopy and multivariate statistical analysis of plasma metabolic phenotypes...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29872406/tongguan-capsule-mitigates-post-myocardial-infarction-remodeling-by-promoting-autophagy-and-inhibiting-apoptosis-role-of-sirt1
#8
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/29858047/mir-93-5p-containing-exosomes-treatment-attenuates-acute-myocardial-infarction-induced-myocardial-damage
#9
Jiwen Liu, Mei Jiang, Shengqiong Deng, Jide Lu, Hui Huang, Yu Zhang, Peihua Gong, Xumin Shen, Huanjun Ruan, Mingming Jin, Hairong Wang
Adipose-derived stromal cells (ADSCs) have been considered as an attractive therapeutic tool. Accumulating evidence indicates that the healing effects of ADSCs are mainly related to paracrine action rather than transdifferentiation. Data show that the expression of miR-93-5p has a cardio-protective effect after acute myocardial infarction (AMI). To identify whether miR-93-5p-encapsulating exosomes that form ADSCs have a better cardio-protective effect, we investigated the inflammatory factors and miR-30d-5p expression in clinical levels...
June 1, 2018: Molecular Therapy. Nucleic Acids
https://www.readbyqxmd.com/read/29858017/by-targeting-atg7-microrna-143-mediates-oxidative-stress-induced-autophagy-of-c-kit-mouse-cardiac-progenitor-cells
#10
Wenya Ma, Fengzhi Ding, Xiuxiu Wang, Qi Huang, Lai Zhang, Chongwei Bi, Bingjie Hua, Ye Yuan, Zhenbo Han, Mengyu Jin, Tianyi Liu, Ying Yu, Benzhi Cai, Zhimin Du
Therapeutic efficiency of cardiac progenitor cells (CPCs) transplantation is limited by its low survival and retention in infarcted myocardium. Autophagy plays a critical role in regulating cell death and apoptosis, but the role of microRNAs (miRNAs) in oxidative stress-induced autophagy of CPCs remains unclear. This study aimed to explore if miRNAs mediate autophagy of c-kit+ CPCs. We found that the silencing of miR-143 promoted the autophagy of c-kit+ CPCs in response to H2 O2 , and the protective effect of miR-143 inhibitor was abrogated by autophagy inhibitor 3-methyladenine (3-MA)...
May 29, 2018: EBioMedicine
https://www.readbyqxmd.com/read/29849901/exendin-4-and-liraglutide-attenuate-glucose-toxicity-induced-cardiac-injury-through-mtor-ulk1-dependent-autophagy
#11
Wei Yu, Wenliang Zha, Jun Ren
Mitochondrial injury and defective autophagy are common in diabetic cardiomyopathy. Recent evidence supports benefits of glucagon-like peptide-1 (GLP-1) agonists exendin-4 (Exe) and liraglutide (LIRA) against diabetic cardiomyopathy. This study was designed to examine the effect of Exe and LIRA on glucose-induced cardiomyocyte and mitochondrial injury, oxidative stress, apoptosis, and autophagy change. Cardiomyocytes isolated from adult mice and H9c2 myoblast cells were exposed to high glucose (HG, 33 mM) with or without Exe or LIRA...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29849149/disruption-of-the-beclin-1-bcl2-autophagy-regulatory-complex-promotes-longevity-in-mice
#12
Álvaro F Fernández, Salwa Sebti, Yongjie Wei, Zhongju Zou, Mingjun Shi, Kathryn L McMillan, Congcong He, Tabitha Ting, Yang Liu, Wei-Chung Chiang, Denise K Marciano, Gabriele G Schiattarella, Govind Bhagat, Orson W Moe, Ming Chang Hu, Beth Levine
Autophagy increases the lifespan of model organisms; however, its role in promoting mammalian longevity is less well-established1,2 . Here we report lifespan and healthspan extension in a mouse model with increased basal autophagy. To determine the effects of constitutively increased autophagy on mammalian health, we generated targeted mutant mice with a Phe121Ala mutation in beclin 1 (Becn1F121A/F121A ) that decreases its interaction with the negative regulator BCL2. We demonstrate that the interaction between beclin 1 and BCL2 is disrupted in several tissues in Becn1 F121A/F121A knock-in mice in association with higher levels of basal autophagic flux...
May 30, 2018: Nature
https://www.readbyqxmd.com/read/29845269/molecular-mechanisms-of-autophagy-in-cardiac-ischemia-reperfusion-injury-review
#13
Xiao-Long Lin, Wei-Jin Xiao, Le-Le Xiao, Mi-Hua Liu
Autophagy is a maintenance process for recycling long-lived proteins and cytoplasmic organelles. The level of this process is enhanced during ischemia/reperfusion (I/R) injury. Autophagy can trigger survival signaling in myocardial ischemia, whereas defective autophagy during reperfusion is detrimental. Autophagy can be regulated through multiple signaling pathways in I/R, including Beclin‑1/class III phosphatidylinositol‑3 kinase (PI‑3K), adenosine monophosphate activated protein kinase/mammalian target of rapamycin (mTOR), and PI‑3K/protein kinase B/mTOR pathways, which consequently lead to different functions...
May 16, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29803339/mitochondrial-calcium-uniporter-inhibition-provides-cardioprotection-in-pressure-overload-induced-heart-failure-through-autophagy-enhancement
#14
Ziqing Yu, Ruizhen Chen, Minghui Li, Yong Yu, Yixiu Liang, Fei Han, Shengmei Qin, Xueying Chen, Yangang Su, Junbo Ge
BACKGROUND: HF incurs high disease burden, and the effectiveness of known HF treatments is unsatisfactory. Therefore, seeking novel therapeutic target of HF is important. The present study aimed to investigate the role of the mitochondrial calcium uniporter (MCU) and its relationship with autophagy in overload-induced heart failure (HF). METHODS AND RESULTS: In both early-stage and end-stage of pressure overload-induced HF, MCU appeared up-regulated along with heart enlargement, increased microtubule-associated proteins 1A/1B light chain 3B (LC3B) II/I ratio and autophagosome content, damaged cardiac function, and ventricular asynchrony...
May 20, 2018: International Journal of Cardiology
https://www.readbyqxmd.com/read/29800228/pcsk9-expression-in-the-ischemic-heart-and-its-relationship-to-infarct-size-cardiac-function-and-development-of-autophagy
#15
Zufeng Ding, Xianwei Wang, Shijie Liu, Jiwani Shahanawaz, Sue Theus, Yubo Fan, Xiaoyan Deng, Sichang Zhou, Jawahar L Mehta
Background: Inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel therapy to treat hypercholesterolemia and related cardiovascular diseases. This study determined if PCSK9 can regulate infarct size, cardiac function and autophagy during ischemia. Methods and Results: Mice hearts were subjected to left coronary artery (LCA) occlusion. There was intense expression of PCSK9 in the zone bordering the infarct area- in association with marked cardiac contractile dysfunction in the wild-type mice...
May 24, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29786779/dnmt3a-controls-mir-200b-in-cardiac-fibroblast-autophagy-and-cardiac-fibrosis
#16
Xu-Dong Zhao, Run-He Qin, Jing-Jing Yang, Sheng-Song Xu, Hui Tao, Xuan-Sheng Ding, Kai-Hu Shi
AIM AND OBJECTIVE: Regulation of microRNA gene expression by DNA methylation may represent a key mechanism to drive cardiac fibrosis progression. Cardiac fibroblast autophagy is the primary source of cardiac fibrosis, but the mechanisms underlying this process are incompletely understood. Here we found that DNMT3A suppression of the microRNA-200b (miR-200b) through pathway leads to cardiac fibroblast autophagy in cardiac fibrosis. METHODS: To understand the impact of DNMT3A on miR-200b at cardiac fibrosis, the rat cardiac fibrosis model was established via the abdominal aortic coarctation...
May 21, 2018: Inflammation Research: Official Journal of the European Histamine Research Society ... [et Al.]
https://www.readbyqxmd.com/read/29774216/autophagic-regulation-of-lipid-homeostasis-in-cardiometabolic-syndrome
#17
Mingjie Yang, Yingmei Zhang, Jun Ren
As an important protein quality control process, autophagy is essential for the degradation and removal of long-lived or injured cellular components and organelles. Autophagy is known to participate in a number of pathophysiological processes including cardiometabolic syndrome. Recent findings have shown compelling evidence for the intricate interplay between autophagy and lipid metabolism. Autophagy serves as a major regulator of lipid homeostasis while lipid can also influence autophagosome formation and autophagic signaling...
2018: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29772440/inhibition-of-nogo-b-promotes-cardiac-hypertrophy-via-endoplasmic-reticulum-stress
#18
Junli Li, Wenchao Wu, Yanguo Xin, Mingyue Zhao, Xiaojing Liu
AIMS: Nogo-B is a key endoplasmic reticulum (ER) protein that regulates ER stress signaling. However, its role in cardiac hypertrophy remains poorly understood. ER stress is interrelated with autophagy in the process of cardiac hypertrophy. Therefore, we aimed to test the hypothesis that both ER stress and autophagy signaling mediate the function of Nogo-B in cardiac hypertrophy. MAIN METHODS: Rat models of transverse aortic constriction (TAC), neonatal rat cardiomyocytes (NRCMs) stimulated with norepinephrine (Ne) and primary cardiac fibroblasts treated with transforming growth factor β1 (TGF-β1) were used in this study...
May 14, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29765503/oleuropein-aglycone-protects-against-mao-a-induced-autophagy-impairment-and-cardiomyocyte-death-through-activation-of-tfeb
#19
Caterina Miceli, Yohan Santin, Nicola Manzella, Raffaele Coppini, Andrea Berti, Massimo Stefani, Angelo Parini, Jeanne Mialet-Perez, Chiara Nediani
Age-associated diseases such as neurodegenerative and cardiovascular disorders are characterized by increased oxidative stress associated with autophagy dysfunction. Oleuropein aglycone (OA), the main polyphenol found in olive oil, was recently characterized as an autophagy inducer and a promising agent against neurodegeneration. It is presently unknown whether OA can have beneficial effects in a model of cardiac stress characterized by autophagy dysfunction. Here, we explored the effects of OA in cardiomyocytes with overexpression of monoamine oxidase-A (MAO-A)...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29762537/the-cardioprotective-effect-of-metformin-in-doxorubicin-induced-cardiotoxicity-the-role-of-autophagy
#20
Rita Zilinyi, Attila Czompa, Andras Czegledi, Andrea Gajtko, Dora Pituk, Istvan Lekli, Arpad Tosaki
The molecular mechanisms underlying doxorubicin-induced cardiotoxicity are still being investigated, but are known to involve oxidative stress, mitochondrial dysfunction, and the dysregulation of autophagy. The objective of the current study was to examine the protective role of metformin and its effect on autophagy in doxorubicin-induced cardiotoxicity. Sprague⁻Dawley rats were divided into four groups at random. The doxorubicin-treated group received doxorubicin (3 mg/kg every second day) intraperitoneally...
May 15, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
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