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heart failure and autophagy

Shivika S Gupta, Matthew R Zeglinski, Sunil G Rattan, Natalie M Landry, Saeid Ghavami, Jeffrey T Wigle, Thomas Klonisch, Andrew J Halayko, Ian M C Dixon
The incidence of heart failure with concomitant cardiac fibrosis is very high in developed countries. Fibroblast activation in heart is causal to cardiac fibrosis as they convert to hypersynthetic cardiac myofibroblasts. There is no known treatment for cardiac fibrosis. Myofibroblasts contribute to the inappropriate remodeling of the myocardial interstitium, which leads to reduced cardiac function and ultimately heart failure. Elevated levels of autophagy have been linked to stress-induced ventricular remodeling and other cardiac diseases...
October 1, 2016: Oncotarget
Antoine Heni Chaanine, Erik Kohlbrenner, Scott I Gamb, Adam J Guenzel, Katherine A Klaus, Ahmed U Fayyaz, K Sreekumaran Nair, Roger J Hajjar, Margaret M Redfield
The Forkhead box O3a (FOXO3a) transcription factor has been shown to regulate glucose metabolism, muscle atrophy and cell death in post-mitotic cells. Its role in regulating mitochondrial and myocardial function is not well studied. Based on previous work, we hypothesized that FOXO3a, through BNIP3, modulates mitochondrial morphology and function in HF. We modulated the FOXO3a-BNIP3 pathway in normal and phenylephrine (PE) stressed adult cardiac myocytes (ACM) in vitro and developed a cardiotropic adeno-associated virus serotype 9 encoding dominant-negative FOXO3a (AAV9...
September 30, 2016: American Journal of Physiology. Heart and Circulatory Physiology
Shashi Kumar Gupta, Ariana Foinquinos, Sabrina Thum, Janet Remke, Karina Zimmer, Christophe Bauters, Pascal de Groote, Reinier A Boon, Leon J de Windt, Sebastian Preissl, Lutz Hein, Sandor Batkai, Florence Pinet, Thomas Thum
BACKGROUND: Aging populations show higher incidences of myocardial infarction (MI) and heart failure (HF). Cardiac remodeling post-MI leads to progressive impaired cardiac function caused by a disarray of several processes including derailed autophagy. Microribonucleic acids (miRNAs) are known to be key players in cardiovascular disease but their involvement in cardiac autophagy and aging is not well understood. OBJECTIVES: This study sought to identify new miRNA candidates that regulate cardiac autophagy and aging...
October 4, 2016: Journal of the American College of Cardiology
Yee-Ki Lee, Yu Jiang, Xin-Ru Ran, Yee-Man Lau, Kwong-Man Ng, Wing-Hon Kevin Lai, Chung-Wah Siu, Hung-Fat Tse
Laminopathy is a disease closely related to deficiency of the nuclear matrix protein lamin A/C or failure in prelamin A processing, and leads to accumulation of the misfold protein causing progeria. The resultant disrupted lamin function is highly associated with abnormal nuclear architecture, cell senescence, apoptosis, and unstable genome integrity. To date, the effects of loss in nuclear integrity on the susceptible organ, striated muscle, have been commonly associated with muscular dystrophy, dilated cardiac myopathy (DCM), and conduction defeats, but have not been studied intensively...
2016: Stem Cell Research & Therapy
Lei Lai, Ningfu Wang, Gangjie Zhu, Xu Duan, Feng Ling
OBJECTIVE: miRNAs are a class of small non-coding RNAs that has been proved to be involved in cardioprotection. The present study was to detect role of miR-30e in cardiac-protective action of ACE2 (angiotensin-converting enzyme 2). METHODS: Sprague Dawley rats were divided into 3 groups and received treatment for a total of 6weeks: group1, normal rats; group2, Doxorubicin-induced heart cardiomyopathy (DHC) rats; and group3, rhACE2 (recombinant human ACE2) treated DHC rats...
September 12, 2016: Life Sciences
Xun Yuan, Yi-Chuan Xiao, Gui-Ping Zhang, Ning Hou, Xiao-Qian Wu, Wen-Liang Chen, Jian-Dong Luo, Gen-Shui Zhang
Diabetes is a potent risk factor for heart failure with preserved ejection fraction (HFpEF). Autophagy can be activated under pathological conditions, including diabetic cardiomyopathy. The therapeutic effects of chloroquine (CQ), an autophagy inhibitor, on left ventricle function in streptozotocin (STZ)-induced diabetic mice were investigated. The cardiac function, light chain 3 (LC3)-II/LC3-I ratio, p62, beclin 1, reactive oxygen species, apoptosis, and fibrosis were measured 14 days after CQ (ip 60 mg/kg/d) administration...
2016: Drug Design, Development and Therapy
Lichun Zhou, Baohua Ma, Xiuzhen Han
Pathological cardiac hypertrophy is associated with nearly all forms of heart failure. It develops in response to disorders such as coronary artery disease, hypertension and myocardial infarction. Angiotensin II (Ang II) has direct effects on the myocardium and promotes hypertension. Chronic elevation of Ang II can lead to pathological cardiac hypertrophy and cardiac failure. Autophagy is an important process in the pathogenesis of cardiovascular diseases. Under physiological conditions, autophagy is an essential homeostatic mechanism to maintain the global cardiac structure function by ridding damaged cells or unwanted macromolecules and organelles...
November 2016: Journal of Molecular Endocrinology
Ming Su, Zhiguo Chen, Changxin Wang, Lei Song, Yubao Zou, Lianfeng Zhang, Rutai Hui, Jizheng Wang
BACKGROUND: MicroRNAs play a crucial role in the regulation of pathological cardiac remodeling and heart failure. Previously, we found that overexpression of miR-221 induces heart failure in mice. The miR-222 and miR-221 share the same gene cluster, however, the role of miR-222 in the regulation of cardiac function remained ill-defined. METHODS AND RESULTS: Transgenic mice with cardiac-specific expression of miR-222 (Tg-miR-222) mice were generated. The Tg-miR-222 mice developed significantly enlarged hearts at 4 weeks of age...
2016: Cellular Physiology and Biochemistry
Hui Li, Yiqing Mao, Qun Zhang, Qing Han, Zhenming Man, Jingyu Zhang, Xi Wang, Ruobi Hu, Xuehui Zhang, David M Irwin, Gang Niu, Huanran Tan
ETHNOPHARMACOLOGICAL RELEVANCE: Using insects, such as the cockroach, for the treatment of disease has a long history in traditional Chinese medicine. Xinmailong (XML) Injection, a bioactive composite extracted from Periplaneta americana (a species of cockroach), shows reasonable protective effects against cardiovascular injury and was approved for the use in the treatment of cardiac dysfunction in 2006, yet its cardio protective mechanisms remain unclear. AIM: The present study aims to examine the protective effects of XML against epirubicin-induced cardiotoxicity in vivo and determine its underlying mechanisms...
November 4, 2016: Journal of Ethnopharmacology
Manish K Gupta, Jeffrey Robbins
Cardiac proteins are subject to continuous stress and these intrinsic and extrinsic factors, both physiological and pathological can lead to protein misfolding. If the protein quality control (PQC) pathways are in any way compromised or their activities diminished, intracellular aggregates can form and a proteotoxic environment is generated, which contributes to cardiac disease and heart failure. We studied the role that SUMO post-translational modification plays in a proteotoxic cardiac environment. SUMOylation can have an integral role in controlling flux through the ubiquitin-proteasome system, and expression of the SUMO (small ubiquitin-like modifier) E2 enzyme UBE2I/UBC9 improves cardiac PQC...
August 29, 2016: Autophagy
Debabrata Chowdhury, Dinesh Kumar, Pranjal Sarma, Anjana Devi Tangutur, Manika Pal Bhadra
Prohibitin (PHB) is overtly conserved evolutionarily and ubiquitously expressed protein with pleiotropic functions in diverse cellular compartments. However, regulation and function of these proteins in different cells, tissues and in various diseases is different as evidenced by expression of these proteins which is found to be reduced in heart diseases, kidney diseases, lung disease, Crohn's disease and ulcerative colitis but this protein is highly expressed in diverse cancer diseases. The mechanism by which this protein acts at the molecular level in different subcellular localizations or in different cells or tissues in different conditions (diseases or normal) has remained poorly understood...
August 24, 2016: Current Drug Targets
Tsung-Hsien Chen, Mei-Ru Chen, Tzu-Yin Chen, Tzu-Chin Wu, Shan-Wen Liu, Ching-Han Hsu, Gan-Guang Liou, Yu-Ying Kao, Guo-Chung Dong, Pao-Hsien Chu, Jiunn-Wang Liao, Kurt Ming-Chao Lin
Proteinopathy in the heart which often manifests excessive misfolded/aggregated proteins in cardiac myocytes can result in severe fibrosis and heart failure. Here we developed a mouse model, which transgenically express tetrameric DsRed, a red fluorescent protein (RFP), in an attempt to mimic the pathological mechanisms ofcardiac fibrosis. Whilst DsRed is expressed and forms aggregation in most mouse organs, certain pathological defects are specifically recapitulated in cardiac muscle cells including mitochondria damages, aggresome-like residual bodies, excessive ubiquitinated proteins, and the induction of autophagy...
August 2, 2016: Oncotarget
Jiankai Zhang, Zhangyou He, Wenjian Xiao, Qingqing Na, Tianxiu Wu, Kaixin Su, Xiaojun Cui
BACKGROUND: Hypoxia is a well-known factor in the promotion of apoptosis, which contributes to the development of numerous cardiac diseases, such as heart failure and myocardial infarction. Inhibiting apoptosis is an important therapeutic strategy for the treatment of related heart diseases caused by ischemia/hypoxic injury. Previous studies have demonstrated that BAG3 plays an important role in cardiomyocyte apoptosis and survival. However, the role of BAG3 in hypoxia-induced cardiomyocyte apoptosis remains to be clarified...
2016: Cellular Physiology and Biochemistry
Farzaneh G Tahrir, Tijana Knezevic, Manish K Gupta, Jennifer Gordon, Joseph Y Cheung, Arthur M Feldman, Kamel Khalili
Mitochondrial abnormalities impact the development of myofibrillar myopathies. Therefore, understanding the mechanisms underlying the removal of dysfunctional mitochondria from cells is of great importance toward understanding the molecular events involved in the genesis of cardiomyopathy. Earlier studies have ascribed a role for BAG3 in the development of cardiomyopathy in experimental animals leading to the identification of BAG3 mutations in patients with heart failure which may play a part in the onset of disease development and progression...
July 6, 2016: Journal of Cellular Physiology
Jaime A Riquelme, Myra N Chavez, David Mondaca-Ruff, Mario Bustamante, Jose Miguel Vicencio, Andrew F G Quest, Sergio Lavandero
INTRODUCTION: Myocardial infarction (MI) is the leading cause of death. When MI is not lethal, heart failure (HF) is a major consequence with high prevalence and poor prognosis. The targeting of autophagy represents a potentially therapeutic approach for the treatment of both pathologies. AREAS COVERED: PubMed searches were performed to discuss the current state of the art regarding the role of autophagy in MI and HF. We review available and potential approaches to modulate autophagy from a pharmacological and genetic perspective...
September 2016: Expert Review of Cardiovascular Therapy
Ippei Shimizu, Tohru Minamino
The heart must continuously pump blood to supply the body with oxygen and nutrients. To maintain the high energy consumption required by this role, the heart is equipped with multiple complex biological systems that allow adaptation to changes of systemic demand. The processes of growth (hypertrophy), angiogenesis, and metabolic plasticity are critically involved in maintenance of cardiac homeostasis. Cardiac hypertrophy is classified as physiological when it is associated with normal cardiac function or as pathological when associated with cardiac dysfunction...
August 2016: Journal of Molecular and Cellular Cardiology
Shuyi Wang, Xiaoling Zhu, Lize Xiong, Yingmei Zhang, Jun Ren
Paraquat, a quarternary nitrogen herbicide, is a toxic prooxidant leading to multi-organ failure including the heart although the underlying mechanism remains poorly understood. This study was designed to examine the role of the innate proinflammatory mediator toll-like receptor 4 (TLR4) in paraquat-induced cardiac contractile anomalies and the underlying mechanisms involved with a focus on autophagy, a conservative machinery governing protein and organelle degradation and recycling for cardiac homeostasis...
August 22, 2016: Toxicology Letters
Adam R Wende, Martin E Young, John Chatham, Jianhua Zhang, Namakkal S Rajasekaran, Victor M Darley-Usmar
Understanding molecular mechanisms that underlie the recent emergence of metabolic diseases such as diabetes and heart failure has revealed the need for a multi-disciplinary research integrating the key metabolic pathways which change the susceptibility to environmental or pathologic stress. At the physiological level these include the circadian control of metabolism which aligns metabolism with temporal demand. The mitochondria play an important role in integrating the redox signals and metabolic flux in response to the changing activities associated with chronobiology, exercise and diet...
May 27, 2016: Free Radical Biology & Medicine
Bao Li, Rui-Fang Chi, Fu-Zhong Qin, Xiao-Fei Guo
What is the central question of this study? We investigated the changes of myocyte autophagy during the stages of myocardial hypertrophy and failure and the relationship between autophagy and oxidative stress. What is the main findings and its importance? Myocyte autophagy is reduced during myocardial hypertrophy and increased during heart failure. Reduced autophagy is correlated with myocyte hypertrophy, and increased autophagy is correlated with myocyte apoptosis. The distinct alterations are associated with oxidative stress...
August 1, 2016: Experimental Physiology
Wenju Li, Xiaoli Li, Bin Wang, Yan Chen, Aiping Xiao, Di Zeng, Dongbo Ou, Song Yan, Wei Li, Qiangsun Zheng
Diabetic cardiomyopathy increases the risk for the development of heart failure independent of coronary artery disease and hypertension. Either type 1 or type 2 diabetes is often accompanied by varying degrees of hyperglycemia, which has been proven to induce myocardial apoptosis in animal models. Recently, a novel small molecule, ZLN005, has been reported to show antidiabetic efficacy in a mouse model, possibly by induction of PGC-1α expression. In this study, we investigated whether ZLN005 protects cardiomyocytes against high glucose-induced cytotoxicity and the mechanisms involved...
July 1, 2016: Experimental Cell Research
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