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heart failure and autophagy

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https://www.readbyqxmd.com/read/29157081/regulation-of-becn1-mediated-autophagy-by-hspb6-insights-from-a-human-hspb6-s10f-mutant
#1
Guan-Sheng Liu, Hongyan Zhu, Wen-Feng Cai, Xiaohong Wang, Min Jiang, Kobina Essandoh, Elizabeth Vafiadaki, Kobra Haghighi, Chi Keung Lam, George Gardner, George Adly, Persoulla Nicolaou, Despina Sanoudou, Qiangrong Liang, Jack Rubinstein, Guo-Chang Fan, Evangelia G Kranias
HSPB6/Hsp20 (heat shock protein family B [small] member 6) has emerged as a novel cardioprotector against stress-induced injury. We identified a human mutant of HSPB6 (HSPB6(S10F)) exclusively present in dilated cardiomyopathy (DCM) patients. Cardiac expression of this mutant in mouse hearts resulted in remodeling and dysfunction, which progressed to heart failure and early death. These detrimental effects were associated with reduced interaction of mutant HSPB6(S10F) with BECN1/Beclin 1, leading to BECN1 ubiquitination and its proteosomal degradation...
November 20, 2017: Autophagy
https://www.readbyqxmd.com/read/29141547/cardioprotective-effects-of-serca2a-overexpression-against-ischemia-reperfusion-induced-injuries-in-rats
#2
Yan Jian, Li-Li Tian, Lin-Hui Wang, Xiao-Dong Zhao, Jing-Wei Chen, Koji Murao, Wei Zhu, Liang Dong, Guo-Qing Wang, Wan-Ping Sun, Guo-Xing Zhang
AIMS: The aim of the present study is to assess how genetically increased Sarcoplasmic reticulum Ca2+-ATPase (Serca2a) expression affects cardiac injury after ischemia/reperfusion (I/R) exposure and the related mechanisms involved. METHODS AND RESULTS: Rats were subjected to left anterior descending coronary artery (LAD) occlusion for 30 min followed by a 24-hour reperfusion. Cardiac function analysis revealed that cardiac function dramatically improved in Serca2a transgenic rats (Serca2aTG) rats compared to wild type (WT) rats...
November 10, 2017: Current Gene Therapy
https://www.readbyqxmd.com/read/29137484/the-role-of-endogenous-reactive-oxygen-species-in-cardiac-myocyte-autophagy
#3
J-P Wang, R-F Chi, J Liu, Y-Z Deng, X-B Han, F-Z Qin, B Li
Autophagy is implicated in the maintenance of cardiac homeostasis. Autophagy is activated in heart failure, in which reactive oxygen species (ROS) are increased. Exogenous ROS have been shown to induce cardiomyocyte autophagy alterations. However, little is known about the influences of physiological levels of endogenous ROS on cardiomyocyte autophagy. In the present study, we tested the hypothesis that endogenous ROS in cardiomyocytes play an important role in inducing autophagy. Cultured H9C2 cardiomyocytes or Sprague-Dawley rats were treated with the antioxidant N-acetyl-cysteine (NAC) or the superoxide dismutase mimic tempol under the basal or nutrient deprivation conditions...
November 10, 2017: Physiological Research
https://www.readbyqxmd.com/read/29129702/fkbp8-protects-the-heart-from-hemodynamic-stress-by-preventing-the-accumulation-of-misfolded-proteins-and-endoplasmic-reticulum-associated-apoptosis-in-mice
#4
Tomofumi Misaka, Tomokazu Murakawa, Kazuhiko Nishida, Yosuke Omori, Manabu Taneike, Shigemiki Omiya, Chris Molenaar, Yoshihiro Uno, Osamu Yamaguchi, Junji Takeda, Ajay M Shah, Kinya Otsu
Protein quality control in cardiomyocytes is crucial to maintain cellular homeostasis. The accumulation of damaged organelles, such as mitochondria and misfolded proteins in the heart is associated with heart failure. During the process to identify novel mitochondria-specific autophagy (mitophagy) receptors, we found FK506-binding protein 8 (FKBP8), also known as FKBP38, shares similar structural characteristics with a yeast mitophagy receptor, autophagy-related 32 protein. However, knockdown of FKBP8 had no effect on mitophagy in HEK293 cells or H9c2 myocytes...
November 10, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29127009/nicorandil-alleviates-myocardial-injury-and-post-infarction-cardiac-remodeling-by-inhibiting-mst1
#5
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...
November 7, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29109832/cardioprotective-effect-of-resveratrol-in-a-postinfarction-heart-failure-model
#6
Adam Riba, Laszlo Deres, Balazs Sumegi, Kalman Toth, Eszter Szabados, Robert Halmosi
Despite great advances in therapies observed during the last decades, heart failure (HF) remained a major health problem in western countries. In order to further improve symptoms and survival in patients with heart failure, novel therapeutic strategies are needed. In some animal models of HF resveratrol (RES), it was able to prevent cardiac hypertrophy, contractile dysfunction, and remodeling. Several molecular mechanisms are thought to be involved in its protective effects, such as inhibition of prohypertrophic signaling molecules, improvement of myocardial Ca(2+) handling, regulation of autophagy, and the reduction of oxidative stress and inflammation...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29098619/the-positive-effects-of-exercise-in-chemotherapy-related-cardiomyopathy
#7
Cavarretta Elena, Mastroiacovo Giorgio, Lupieri Annik, Frati Giacomo, Peruzzi Mariangela
Anthracyclines such as doxorubicin, daunorubicin, epirubicin, mitoxantrone and idarubicin, are powerful chemotherapeutic drugs used both in children and adult populations. Their properties made them particularly suitable for a large variety of neoplasms including breast adenocarcinoma, small cell lung cancer and acute leukemia. Early and late anthracycline-induced cardiotoxicity is a well-known phenomenon, and the incidence of heart failure in patients receiving doxorubicin is 2.2%, with a mortality rate over 60% at 2 years...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29069231/myostatin-promotes-distinct-responses-on-protein-metabolism-of-skeletal-and-cardiac-muscle-fibers-of-rodents
#8
L H Manfredi, S Paula-Gomes, N M Zanon, I C Kettelhut
Myostatin is a novel negative regulator of skeletal muscle mass. Myostatin expression is also found in heart in a much less extent, but it can be upregulated in pathological conditions, such as heart failure. Myostatin may be involved in inhibiting protein synthesis and/or increasing protein degradation in skeletal and cardiac muscles. Herein, we used cell cultures and isolated muscles from rats to determine protein degradation and synthesis. Muscles incubated with myostatin exhibited an increase in proteolysis with an increase of Atrogin-1, MuRF1 and LC3 genes...
October 19, 2017: Brazilian Journal of Medical and Biological Research, Revista Brasileira de Pesquisas Médicas e Biológicas
https://www.readbyqxmd.com/read/29063982/role-of-beta-adrenergic-receptors-and-sirtuin-signaling-in-the-heart-during-aging-heart-failure-and-adaptation-to-stress
#9
REVIEW
Regina Celia Spadari, Claudia Cavadas, Ana Elisa T Saturi de Carvalho, Daniela Ortolani, Andre Luiz de Moura, Paula Frizera Vassalo
In the heart, catecholamine effects occur by activation of beta-adrenergic receptors (β-ARs), mainly the beta 1 (β1-AR) and beta 2 (β2-AR) subtypes, both of which couple to the Gs protein that activates the adenylyl cyclase signaling pathway. The β2-ARs can also couple to the Gi protein that counterbalances the effect of the Gs protein on cyclic adenosine monophosphate production and activates the phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. In several cardiovascular disorders, including heart failure, as well as in aging and in animal models of environmental stress, a reduction in the β1/β2-AR ratio and activation of the β2-AR-Gi-PI3K-Akt signaling pathway have been observed...
October 24, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/29063105/the-roles-of-microrna-22-in-myocardial-infarction
#10
Bin-Hai Cong, Xiao-Yan Zhu, Xin Ni
Myocardial infarction (MI) is the leading cause of morbidity and mortality worldwide. The regeneration capacity of the adult mammalian heart is very limited, so that the lost cells are replaced by fibrotic scar. This is followed by remodeling of the surrounding myocardium, which includes cardiac hypertrophy and fibrosis, and makes the ventricular wall thicken and stiffen. This adverse cardiac remodeling leads to impaired cardiac function and eventually leads to heart failure. Extensive studies have revealed that microRNAs (miRNAs) play an essential role in cardiovascular diseases...
October 25, 2017: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/29021349/activation-of-autophagy-ameliorates-cardiomyopathy-in-mybpc3-targeted-knockin-mice
#11
Sonia R Singh, Antonia T L Zech, Birgit Geertz, Silke Reischmann-Düsener, Hanna Osinska, Maksymilian Prondzynski, Elisabeth Krämer, Qinghang Meng, Charles Redwood, Jolanda van der Velden, Jeffrey Robbins, Saskia Schlossarek, Lucie Carrier
BACKGROUND: Alterations in autophagy have been reported in hypertrophic cardiomyopathy (HCM) caused by Danon disease, Vici syndrome, or LEOPARD syndrome, but not in HCM caused by mutations in genes encoding sarcomeric proteins, which account for most of HCM cases. MYBPC3, encoding cMyBP-C (cardiac myosin-binding protein C), is the most frequently mutated HCM gene. METHODS AND RESULTS: We evaluated autophagy in patients with HCM carrying MYBPC3 mutations and in a Mybpc3-targeted knockin HCM mouse model, as well as the effect of autophagy modulators on the development of cardiomyopathy in knockin mice...
October 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/28966332/the-impact-of-autophagy-on-cardiovascular-senescence-and-diseases
#12
REVIEW
Yuichi Sasaki, Yoshiyuki Ikeda, Masaaki Iwabayashi, Yuichi Akasaki, Mitsuru Ohishi
The risk of cardiovascular disease increases with age, causing chronic disability, morbidity, and mortality in the elderly. Cardiovascular aging and disease are characterized by heart failure, cardiac ischemia-reperfusion injury, cardiomyopathy, hypertension, arterial stiffness, and atherosclerosis. As a cell ages, damaged organelles and abnormal proteins accumulate. A system for removing these cytoplasmic substrates is essential for maintaining homeostasis. Autophagy assists tissue homeostasis by forming a pathway by which these substances are degraded...
October 21, 2017: International Heart Journal
https://www.readbyqxmd.com/read/28956198/immunity-inflammation-and-oxidative-stress-in-heart-failure-emerging-molecular-targets
#13
REVIEW
Karam F Ayoub, Naga Venkata K Pothineni, Joshua Rutland, Zufeng Ding, Jawahar L Mehta
PURPOSE: Heart failure (HF) remains a major cause of morbidity and mortality worldwide. Although various therapies developed over the last two decades have shown improved long term outcomes in patients with established HF, there has been little progress in preventing the adverse cardiac remodeling that initiates HF. To fill the gap in treatment, current research efforts are focused on understanding novel mechanisms and signaling pathways. Immune activation, inflammation, oxidative stress, alterations in mitochondrial bioenergetics, and autophagy have been postulated as important pathophysiological events in this process...
September 27, 2017: Cardiovascular Drugs and Therapy
https://www.readbyqxmd.com/read/28945004/tlr3-contributes-to-persistent-autophagy-and-heart-failure-in-mice-after-myocardial-infarction
#14
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...
September 25, 2017: 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
#15
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/28941803/dj-1-activates-autophagy-in-the-repression-of-cardiac-hypertrophy
#16
Ruicong Xue, Jingzhou Jiang, Bin Dong, Weiping Tan, Yu Sun, Jingjing Zhao, Yili Chen, Yugang Dong, Chen Liu
Cardiac hypertrophy is the risk factor of heart failure when the heart is confronted with pressure overload or neurohumoral stimuli. Autophagy, a conserved degradative pathway, is one of the important mechanisms involved in the regulation of cardiac hypertrophy. DJ-1 is a traditional anti-oxidative protein and emerging evidence suggested that DJ-1 might modulate autophagy. However, the regulation of autophagy by DJ-1 in the process of cardiac hypertrophy remains unknown. In our study, we firstly discovered that the expression of DJ-1declined in the process of pressure overload cardiac hypertrophy, and its alteration was parallel with the impairment of autophagy...
November 1, 2017: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/28913665/role-of-noncoding-rnas-in-regulation-of-cardiac-cell-death-and-cardiovascular-diseases
#17
REVIEW
Yanhan Dong, Cuiyun Liu, Yanfang Zhao, Murugavel Ponnusamy, Peifeng Li, Kun Wang
Loss of functional cardiomyocytes is a major underlying mechanism for myocardial remodeling and heart diseases, due to the limited regenerative capacity of adult myocardium. Apoptosis, programmed necrosis, and autophagy contribute to loss of cardiac myocytes that control the balance of cardiac cell death and cell survival through multiple intricate signaling pathways. In recent years, non-coding RNAs (ncRNAs) have received much attention to uncover their roles in cell death of cardiovascular diseases, such as myocardial infarction, cardiac hypertrophy, and heart failure...
September 14, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28874825/knockout-of-the-atpase-inhibitory-factor-1-protects-the-heart-from-pressure-overload-induced-cardiac-hypertrophy
#18
Kevin Yang, Qinqiang Long, Kamalamma Saja, Fengyuan Huang, Steven M Pogwizd, Lufang Zhou, Masasuke Yoshida, Qinglin Yang
Mitochondrial ATP synthase catalyzes the coupling of oxidative phosphorylation. Under pathological conditions, ATP synthase hydrolyzes ATP to replenish protons from the matrix into the intermembrane space, sustaining mitochondrial membrane potential. ATPase inhibitory factor 1 (IF1) is a nuclear-encoded, ATP synthase-interacting protein that selectively inhibits the hydrolysis activity of ATP synthase, which may render the protective role of IF1 in ischemic hearts. However, the in vivo cardiac function of IF1 and the potential therapeutic application targeting IF1 remain obscure...
September 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28871076/knockdown-of-microrna-122-protects-h9c2-cardiomyocytes-from-hypoxia-induced-apoptosis-and-promotes-autophagy
#19
Zaiwei Zhang, Hu Li, Shasha Chen, Ying Li, Zhiyuan Cui, Jie Ma
BACKGROUND Acute myocardial infarction (AMI) is a severe disease causing heart failure and sudden death. Studies indicate that microRNAs (miRNAs) are involved in the pathophysiology of AMI. In the present study, we carefully explored the effects of miR-122 on myocardial hypoxia injury and its possible underlying mechanism. MATERIAL AND METHODS miR-122 expression was analyzed in H9c2 cardiomyocytes after being transfected with miR-122 mimic, ASO-miR-122, or negative control. Cell viability and apoptosis were investigated by CCK-8 assays and flow cytometry analysis, respectively...
September 5, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28842527/mechanisms-contributing-to-cardiac-remodelling
#20
REVIEW
Qing-Qing Wu, Yang Xiao, Yuan Yuan, Zhen-Guo Ma, Hai-Han Liao, Chen Liu, Jin-Xiu Zhu, Zheng Yang, Wei Deng, Qi-Zhu Tang
Cardiac remodelling is classified as physiological (in response to growth, exercise and pregnancy) or pathological (in response to inflammation, ischaemia, ischaemia/reperfusion (I/R) injury, biomechanical stress, excess neurohormonal activation and excess afterload). Physiological remodelling of the heart is characterized by a fine-tuned and orchestrated process of beneficial adaptations. Pathological cardiac remodelling is the process of structural and functional changes in the left ventricle (LV) in response to internal or external cardiovascular damage or influence by pathogenic risk factors, and is a precursor of clinical heart failure (HF)...
September 15, 2017: Clinical Science (1979-)
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