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Cardiac autophagy

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https://www.readbyqxmd.com/read/28079007/novel-therapies-targeting-cardioprotection-and-regeneration
#1
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/28069395/rutin-attenuates-doxorubicin-induced-cardiotoxicity-via-regulating-autophagy-and-apoptosis
#2
Yanyan Ma, Lifang Yang, Jipeng Ma, Linhe Lu, Xiaowu Wang, Jun Ren, Jian Yang
Doxorubicin as anticancer agent can cause dose-dependent cardiotoxicity and heart failure in the long term. Rutin as a polyphenolic flavonoid has been illustrated to protect hearts from diverse cardiovascular diseases. Its function is known to be related to its antioxidant and antiinflammatory activity which may regulate multiple cellular signal pathways. However, the role of rutin on doxorubicin-induced cardiotoxicity has yet to be discovered. In this study, we explored the protective role of rutin on doxorubicin-induced heart failure and elucidated the potential mechanisms of protective effects of rutin against cardiomyocyte death...
January 6, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28052027/estrogen-receptor-%C3%AE-ligation-inhibits-hodgkin-lymphoma-growth-by-inducing-autophagy
#3
Marina Pierdominici, Angela Maselli, Silvia L Locatelli, Laura Ciarlo, Giuseppa Careddu, Mario Patrizio, Barbara Ascione, Antonella Tinari, Carmelo Carlo-Stella, Walter Malorni, Paola Matarrese, Elena Ortona
Although Hodgkin lymphoma (HL) is curable with current therapy, at least 20% of patients relapse or fail to make complete remission. In addition, patients who achieve long-term disease-free survival frequently undergo infertility, secondary malignancies, and cardiac failure, which are related to chemotherapeutic agents and radiation therapies. Hence, new therapeutic strategies able to counteract the HL disease in this important patient population are still a matter of study. Estrogens, in particular 17β-estradiol (E2), have been suggested to play a role in lymphoma cell homeostasis by estrogen receptors (ER) β activation...
December 28, 2016: Oncotarget
https://www.readbyqxmd.com/read/28007739/ischemic-preconditioning-confers-epigenetic-repression-of-mtor-and-induction-of-autophagy-through-g9a-dependent-h3k9-dimethylation
#4
Olof Gidlöf, Andrea L Johnstone, Kerstin Bader, Bohdan B Khomtchouk, Jiaqi J O'Reilly, Selvi Celik, Derek J Van Booven, Claes Wahlestedt, Bernhard Metzler, David Erlinge
BACKGROUND: Ischemic preconditioning (IPC) protects the heart from prolonged ischemic insult and reperfusion injury through a poorly understood mechanism. Post-translational modifications of histone residues can confer rapid and drastic switches in gene expression in response to various stimuli, including ischemia. The aim of this study was to investigate the effect of histone methylation in the response to cardiac ischemic preconditioning. METHODS AND RESULTS: We used cardiac biopsies from mice subjected to IPC to quantify global levels of 3 of the most well-studied histone methylation marks (H3K9me2, H3K27me3, and H3K4me3) with Western blot and found that H3K9me2 levels were significantly increased in the area at risk compared to remote myocardium...
December 22, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27998869/-role-of-autophagy-in-fasudil-induced-rho-kinase-inhibition-for-protection-against-myocardial-ischemia-reperfusion-injury-in-rats
#5
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/27997746/autophagy-an-adaptive-physiological-countermeasure-to-cellular-senescence-and-ischaemia-reperfusion-associated-cardiac-arrhythmias
#6
REVIEW
Istvan Lekli, David Donald Haines, Gyorgy Balla, Arpad Tosaki
Oxidative stress placed on tissues that involved in pathogenesis of a disease activates compensatory metabolic changes, such as DNA damage repair that in turn causes intracellular accumulation of detritus and 'proteotoxic stress', leading to emergence of 'senescent' cellular phenotypes, which express high levels of inflammatory mediators, resulting in degradation of tissue function. Proteotoxic stress resulting from hyperactive inflammation following reperfusion of ischaemic tissue causes accumulation of proteinaceous debris in cells of the heart in ways that cause potentially fatal arrhythmias, in particular ventricular fibrillation (VF)...
December 20, 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27994061/focal-adhesion-kinase-mediated-phosphorylation-of-beclin1-suppresses-cardiomyocyte-autophagy-and-initiates-hypertrophic-growth
#7
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. While 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...
December 19, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27981013/plga-pnipam-microspheres-loaded-with-the-gastrointestinal-nutrient-nab-ameliorate-cardiac-dysfunction-by-activating-sirt3-in-acute-myocardial-infarction
#8
Panke Cheng, Wen Zeng, Li Li, Da Huo, Lingqing Zeng, Ju Tan, Jingting Zhou, Jiansen Sun, Ge Liu, Yanzhao Li, Ge Guan, Yuxin Wang, Chuhong Zhu
Acute myocardial infarction (AMI) is the death of cardiomyocytes caused by a lack of energy due to ischemia. Nutrients supplied by the blood are the main source of cellular energy for cardiomyocytes. Sodium butyrate (NaB), a gastrointestinal nutrient, is a short-chain fatty acid (butyric acid) that may act as an energy source in AMI therapy. Poly(lactic-co-glycolic acid)-Poly (N-isopropylacrylamide) microspheres loaded with NaB (PP-N) are synthesized to prolong the release of NaB and are injected into ischemic zones in a Sprague-Dawley rat AMI model...
December 2016: Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
https://www.readbyqxmd.com/read/27973540/bicarbonate-increases-ischemia-reperfusion-damage-by-inhibiting-mitophagy
#9
Bruno B Queliconi, Alicia J Kowaltowski, Roberta A Gottlieb
During an ischemic event, bicarbonate and CO2 concentration increase as a consequence of O2 consumption and lack of blood flow. This event is important as bicarbonate/CO2 is determinant for several redox and enzymatic reactions, in addition to pH regulation. Until now, most work done on the role of bicarbonate in ischemia-reperfusion injury focused on pH changes; although reperfusion solutions have a fixed pH, cardiac resuscitation protocols commonly employ bicarbonate to correct the profound acidosis associated with respiratory arrest...
2016: PloS One
https://www.readbyqxmd.com/read/27967213/could-nlrp3-inflammasome-be-a-cardiovascular-risk-biomarkers-in-acute-myocardial-infarction-patients
#10
Pedro Bullon, Francisco J Cano-García, Elisabet Alcocer-Gómez, Alfonso Varela-Lopez, Lourdes Román-Malo, Rafael J Ruiz-Salmerón, Jose L Quiles, Jose M Navarro-Pando, Maurizio Battino, Jesús Ruiz-Cabello, Luis J Jiménez-Borreguero, Mario D Cordero
Conventional cardiovascular risk factors (CVRF) are accepted to identify asymptomatic individuals with high risk of acute myocardial infarction (AMI). However, AMI affects many patients previously classified at low risk. New biomarkers are needed to improve risk prediction. We propose to evaluate the NLRP3-inflammasome complex as a potential CVR indicator in healthy males and post-AMI patients and compare both groups by known CVRFs. We included 109 men with no history of cardiovascular disease (controls) and 150 AMI patients attending a cardiac rehabilitation program...
December 14, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27959392/syringin-prevents-cardiac-hypertrophy-induced-by-pressure-overload-through-the-attenuation-of-autophagy
#11
Fangfang Li, Ning Zhang, Qingqing Wu, Yuan Yuan, Zheng Yang, Mengqiao Zhou, Jinxiu Zhu, Qizhu Tang
Syringin, extracted from Eleutherococcus senticosus, is a major biologically active component of Chinese herbs. Studies have certified the multiple pharmacological properties of syringin. However, the role of syringin in cardiac hypertrophy and the mechanisms involved remain unclear. In this study, aortic banding was performed on mice in order to induce cardiac hypertrophy, and the animals were then treated with syringin for 7 weeks. Echocardiography and catheter-based measurements of hemodynamic parameters were performed to evaluate cardiac function at 8 weeks following aortic banding...
January 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/27916343/cardiac-autophagic-vacuolation-in-severe-x-linked-myopathy-with-excessive-autophagy
#12
Iulia Munteanu, Hannu Kalimo, Antti Saraste, Ichizo Nishino, Berge A Minassian
X-linked myopathy with excessive autophagy (XMEA), caused by mutations of the VMA21 gene, is a strictly skeletal muscle disease. Extensive studies in yeast established VMA21 as the master assembly chaperone of V-ATPase, the complex multisubunit proton pump that acidifies organelles and that is vital to all mammalian tissues. As such, skeletal muscle disease exclusivity in XMEA is highly surprising. We now show that the severest VMA21 mutation, c.164-6t>g, does result in XMEA-typical pathology with autophagic vacuolar changes outside skeletal muscle, namely in the heart...
October 19, 2016: Neuromuscular Disorders: NMD
https://www.readbyqxmd.com/read/27904666/ad-hgf-improves-the-cardiac-remodeling-of-rat-following-myocardial-infarction-by-upregulating-autophagy-and-necroptosis-and-inhibiting-apoptosis
#13
Jiabao Liu, Peng Wu, Yunle Wang, Yingqiang Du, Nan A, Shuiyuan Liu, Yiming Zhang, Ningtian Zhou, Zhihui Xu, Zhijian Yang
Cell death in MI is the most critical determinant of subsequent left ventricular remodeling and heart failure. Besides apoptosis, autophagy and necroptosis have been recently found to be another two regulated cell death styles. HGF has been reported to have a protective role in MI, but its impact on the three death styles remains unclear. Thus, our study was performed to investigate the distribution of autophagy, apoptosis and necroptosis in cardiac tissues after MI and explore the role and mechanism of Ad-HGF on cardiac remodeling by regulating the three death styles...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27897112/harnessing-the-power-of-sirt1-and-non-coding-rnas-in-vascular-disease
#14
Kenneth Maiese
Noncommunicable diseases (NCDs) contribute to a significant amount of disability and death in the world. Of these disorders, vascular disease is ranked high, falls within the five leading causes of death, and impacts multiple other disease entities such as those of the cardiac system, nervous system, and metabolic disease. Targeting the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) pathway and the modulation of micro ribonucleic acids (miRNAs) may hold great promise for the development of novel strategies for the treatment of vascular disease since each of these pathways are highly relevant to cardiac and nervous system disorders as well as to metabolic dysfunction...
November 29, 2016: Current Neurovascular Research
https://www.readbyqxmd.com/read/27889531/sirt1-protects-cardiac-cells-against-apoptosis-induced-by-zearalenone-or-its-metabolites-%C3%AE-and-%C3%AE-zearalenol-through-an-autophagy-dependent-pathway
#15
Intidhar Ben Salem, Manel Boussabbeh, Julie Pires Da Silva, Arnaud Guilbert, Hassen Bacha, Salwa Abid-Essefi, Christophe Lemaire
Zearalenone (ZEN) is a non-steroidal estrogenic mycotoxin produced by several species of Fusarium in cereals and agricultural products. The major ZEN metabolites are α-zearalenol (α-ZOL) and β-zearalenol (β-ZOL). In the present study, we investigated the underlying mechanism of the toxicity induced by ZEN, α-ZOL and β-ZOL in cardiac cells (H9c2). We show that treatment with ZEN or its metabolites induces the activation of the mitochondrial pathway of apoptosis as characterized by an increase in ROS generation, a loss of mitochondrial transmembrane potential (ΔΨm) and an activation of caspases...
January 1, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/27882354/bcl-2-associated-athanogene-3-protects-the-heart-from-ischemia-reperfusion-injury
#16
Feifei Su, Valerie D Myers, Tijana Knezevic, JuFang Wang, Erhe Gao, Muniswamy Madesh, Farzaneh G Tahrir, Manish K Gupta, Jennifer Gordon, Joseph Rabinowitz, Frederick V Ramsey, Douglas G Tilley, Kamel Khalili, Joseph Y Cheung, Arthur M Feldman
Bcl-2-associated athanogene 3 (BAG3) is an evolutionarily conserved protein expressed at high levels in the heart and the vasculature and in many cancers. While altered BAG3 expression has been associated with cardiac dysfunction, its role in ischemia/reperfusion (I/R) is unknown. To test the hypothesis that BAG3 protects the heart from reperfusion injury, in vivo cardiac function was measured in hearts infected with either recombinant adeno-associated virus serotype 9-expressing (rAAV9-expressing) BAG3 or GFP and subjected to I/R...
November 17, 2016: JCI Insight
https://www.readbyqxmd.com/read/27880725/mouse-sirt3-promotes-autophagy-in-angii-induced-myocardial-hypertrophy-through-the-deacetylation-of-foxo1
#17
Jingyuan Li, Tongshuai Chen, Ming Xiao, Na Li, Shujian Wang, Hongyan Su, Xiaobin Guo, Hui Liu, Fangying Yan, Yi Yang, Yun Zhang, Peili Bu
Sirt3, a mitochondrial NAD+-dependent histone deacetylase, is the only member proven to promote longevity in mammalian Sirtuin family. The processed short form of Sirt3 has been demonstrated to target many mediators of energy metabolism and mitochondrial stress adaptive program. Autophagy serves as a dynamic recycling mechanism and provides energy or metabolic substrates. Among the mechanisms triggered by cardiac stress, opinions vary as to whether autophagy is a protective or detrimental response. Here, by inducing the Sirt3-knockout mice to myocardial hypertrophy with chronic angiotensin II infusion for four weeks, we determined the role of Sirt3 in myocardial hypertrophy and autophagy...
November 17, 2016: Oncotarget
https://www.readbyqxmd.com/read/27865838/helix-b-surface-peptide-attenuates-diabetic-cardiomyopathy-via-ampk-dependent-autophagy
#18
Chen Lin, Mingming Zhang, Yingmei Zhang, Kejian Yang, Jianqiang Hu, Rui Si, Guoyong Zhang, Beilei Gao, Xiang Li, Chennian Xu, Congye Li, Qimeng Hao, Wenyi Guo
BACKGROUND: Erythropoietin (EPO) has been reported to exert protective effects on a host of damaged tissues. However, the erythropoietic effect of this hormone can result in high risks of thrombosis, stroke, and hypertension, remarkably limiting the clinical use of EPO. Helix B surface peptide (HBSP) is a small peptide derived from the helix-B domain of EPO. Surprisingly, HBSP retains the tissue protective properties of EPO without altering the hematocrit. Thus, we evaluated the possible role of HBSP on diabetic cardiomyopathy...
January 22, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27863349/trpv1-channels-in-cardiovascular-system-a-double-edged-sword
#19
REVIEW
Puneet Kaur Randhawa, Amteshwar Singh Jaggi
Apart from modulating nociception, there is vital role of TRPV1 channels in modulating atherosclerosis, congestive heart failure, systemic hypertension, pulmonary hypertension, hemorrhagic shock and vascular remodeling. TRPV1 channel activation has shielding effect against the development of atherosclerosis and systemic hypertension. TRPV1 channel activation alleviates the formation of atherosclerotic lesions via increasing the expression of cholesterol efflux regulatory protein, UCP 2 and enhancing autophagy...
February 1, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/27862268/novel-protective-role-of-nuclear-melatonin-receptor-ror%C3%AE-in-diabetic-cardiomyopathy
#20
Yichao Zhao, Longwei Xu, Song Ding, Nan Lin, Qingqi Ji, Lingchen Gao, Yuanyuan Su, Jun Pu, Ben He
Diabetic cardiomyopathy is a major complication that significantly contributes to morbidity and mortality in diabetics with few therapies. Moreover, anti-diabetic drugs reported inconsistent or even adverse cardiovascular effects, suggesting it is important to exploit novel therapeutic targets against diabetic cardiomyopathy. Here, we observed that the nuclear melatonin receptor, the retinoic acid-related orphan receptor α (RORα), was downregulated in diabetic hearts. By utilizing a mouse line with RORα disruption, we demonstrated that RORα deficiency led to significantly augmented diastolic dysfunction and cardiac remodeling induced by diabetes...
November 18, 2016: Journal of Pineal Research
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