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heart failure and autophagy

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https://www.readbyqxmd.com/read/29761889/a-novel-human-s10f-hsp20-mutation-induces-lethal-peripartum-cardiomyopathy
#1
Guan-Sheng Liu, George Gardner, George Adly, Min Jiang, Wen-Feng Cai, Chi Keung Lam, Fawzi Alogaili, Nathan Robbins, Jack Rubinstein, Evangelia G Kranias
Heat shock protein 20 (Hsp20) has been shown to be a critical regulator of cardiomyocyte survival upon cardiac stress. In this study, we investigated the functional significance of a novel human Hsp20 mutation (S10F) in peripartum cardiomyopathy. Previous findings showed that cardiac-specific overexpression of this mutant were associated with reduced autophagy, left ventricular dysfunction and early death in male mice. However, this study indicates that females have normal function with no alterations in autophagy but died within a week after 1-4 pregnancies...
May 15, 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29737434/anti-apoptosis-in-nonmyocytes-and-pro-autophagy-in-cardiomyocytes-two-strategies-against-postinfarction-heart-failure-through-regulation-of-cell-death-degeneration
#2
REVIEW
Genzou Takemura, Hiromitsu Kanamori, Hideshi Okada, Nagisa Miyazaki, Takatomo Watanabe, Akiko Tsujimoto, Kazuko Goto, Rumi Maruyama, Takako Fujiwara, Hisayoshi Fujiwara
Anti-apoptotic therapy for cardiomyocytes could be an effective strategy for preventing or treating heart failure. Notably, however, morphological evidence definitively demonstrating cardiomyocyte apoptosis has been very rare in actual heart diseases such as acute myocardial infarction and heart failure. By contrast, within the postinfarction heart, interstitial noncardiomyocytes such as granulation tissue cells do die via apoptosis to form scar tissue. Blockade of this apoptosis improves survival and mitigates ventricular remodeling and dysfunction during the chronic stage...
May 8, 2018: Heart Failure Reviews
https://www.readbyqxmd.com/read/29694958/current-mechanistic-concepts-in-ischemia-and-reperfusion-injury
#3
Meng-Yu Wu, Giou-Teng Yiang, Wan-Ting Liao, Andy Po-Yi Tsai, Yeung-Leung Cheng, Pei-Wen Cheng, Chia-Ying Li, Chia-Jung Li
Ischemia-reperfusion injury is associated with serious clinical manifestations, including myocardial hibernation, acute heart failure, cerebral dysfunction, gastrointestinal dysfunction, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. Ischemia-reperfusion injury is a critical medical condition that poses an important therapeutic challenge for physicians. In this review article, we present recent advances focusing on the basic pathophysiology of ischemia-reperfusion injury, especially the involvement of reactive oxygen species and cell death pathways...
2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29625179/proteostasis-in-epicardial-versus-subcutaneous-adipose-tissue-in-heart-failure-subjects-with-and-without-diabetes
#4
A Burgeiro, A C Fonseca, D Espinoza, L Carvalho, N Lourenço, M Antunes, E Carvalho
BACKGROUND: Cardiovascular diseases (CVDs) are leading cause of death and primary cause of morbidity and mortality in diabetic population. Epicardial adipose tissue (EAT) covers the heart's surface and is a source of biomolecules regulating heart and blood vessel physiology. The protective activation of the unfolded protein response (UPR) and autophagy allows the cardiomyocyte reticular network to restore energy and/or nutrient homeostasis and to avoid cell death. However, an excessive or prolonged UPR activation can trigger cell death...
April 3, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29618792/subcutaneous-ehrlich-ascites-carcinoma-mice-model-for-studying-cancer-induced-cardiomyopathy
#5
Sneha Mishra, Ankit Kumar Tamta, Mohsen Sarikhani, Perumal Arumugam Desingu, Shruti M Kizkekra, Anwit Shriniwas Pandit, Shweta Kumar, Danish Khan, Sathees C Raghavan, Nagalingam R Sundaresan
Cardiomyopathy is one of the characteristic features of cancer. In this study, we establish a suitable model to study breast cancer-induced cardiomyopathy in mice. We used Ehrlich Ascites Carcinoma cells to induce subcutaneous tumor in 129/SvJ mice and studied its effect on heart function. In Ehrlich Ascites Carcinoma bearing mice, we found significant reduction in left ventricle wall thickness, ejection fraction, and fractional shortening increase in left ventricle internal diameter. We found higher muscle atrophy, degeneration, fibrosis, expression of cell-adhesion molecules and cell death in tumor-bearing mice hearts...
April 4, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29608885/microrna-223-protects-neonatal-rat-cardiomyocytes-and-h9c2-cells-from-hypoxia-induced-apoptosis-and-excessive-autophagy-via-the-akt-mtor-pathway-by-targeting-parp-1
#6
Xiaoxiao Liu, Yunfei Deng, Yifeng Xu, Wei Jin, Hongli Li
Myocardial infarction (MI), characterized by interruption of blood and oxygen to myocardium, is a common yet fatal cardiovascular event that causes progressive damage to myocardial tissue and eventually leads to heart failure. Previous studies have shown increased expression of microRNA-223 (miR-223) in infarcted myocardial tissues of humans and in rat models of MI. However, the role of miR-223 in cell survival during MI has not been elucidated. Thus, we aimed to investigate whether miR-223 participates in the regulation of cardiac ischemia-induced injury and to elucidate the underlying mechanisms of this process...
May 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29576856/macroautophagy-and-chaperone-mediated-autophagy-in-heart-failure-the-known-and-the-unknown
#7
REVIEW
Rajeshwary Ghosh, J Scott Pattison
Cardiac diseases including hypertrophic and ischemic cardiomyopathies are increasingly being reported to accumulate misfolded proteins and damaged organelles. These findings have led to an increasing interest in protein degradation pathways, like autophagy, which are essential not only for normal protein turnover but also in the removal of misfolded and damaged proteins. Emerging evidence suggests a previously unprecedented role for autophagic processes in cardiac physiology and pathology. This review focuses on the major types of autophagic processes, the genes and protein complexes involved, and their regulation...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29575479/increasing-autophagy-and-blocking-nrf2-suppress-laminopathy-induced-age-dependent-cardiac-dysfunction-and-shortened-lifespan
#8
Shruti Bhide, Adriana S Trujillo, Maureen T O'Connor, Grant H Young, Diane E Cryderman, Sahaana Chandran, Mastaneh Nikravesh, Lori L Wallrath, Girish C Melkani
Mutations in the human LMNA gene cause a collection of diseases known as laminopathies. These include myocardial diseases that exhibit age-dependent penetrance of dysrhythmias and heart failure. The LMNA gene encodes A-type lamins, intermediate filaments that support nuclear structure and organize the genome. Mechanisms by which mutant lamins cause age-dependent heart defects are not well understood. To address this issue, we modeled human disease-causing mutations in the Drosophila melanogaster Lamin C gene and expressed mutant Lamin C exclusively in the heart...
March 25, 2018: Aging Cell
https://www.readbyqxmd.com/read/29574918/ginsenoside-rb1-inhibits-autophagy-through-regulation-of-rho-rock-and-pi3k-mtor-pathways-in-a-pressure-overload-heart-failure-rat-model
#9
Tianrui Yang, Yunbo Miao, Tong Zhang, Ninghui Mu, Libo Ruan, Jinlan Duan, Ying Zhu, Rongping Zhang
OBJECTIVE: This study was designed to explore the relationship between ginsenoside Rb1 (Grb1) and high-load heart failure (HF) in rats. METHODS: The parameters of cardiac systolic function (left ventricular posterior wall thickness (LVPWT), left ventricular internal diastolic diameter (LVID), fraction shortening (FS) and mitral valves (MVs)) of rat hearts in each group were inspected by echocardiogram. The expressions of rat myocardial contractile proteins, autophagy-related proteins and the activation of Rho/ROCK and PI3K/mTOR pathways were detected by Western blot...
June 2018: Journal of Pharmacy and Pharmacology
https://www.readbyqxmd.com/read/29574782/rab9-dependent-autophagy-is-required-for-the-igf-iir-triggering-mitophagy-to-eliminate-damaged-mitochondria
#10
Chih-Yang Huang, Wei-Wen Kuo, Tsung-Jung Ho, Shu-Fen Chiang, Pei-Ying Pai, Jing-Ying Lin, Ding-Yu Lin, Chia-Hua Kuo, Chih-Yang Huang
Mitochondria dysfunction is the major characteristic of mitophagy, which is essential in mitochondrial quality control. However, excessive mitophagy contributes to cell death in a number of diseases, including ischemic stroke and hepatotoxicity. Insulin-like growth factor II (IGF-II) and its receptor (IGF-IIR) play vital roles in the development of heart failure during hypertension. We found that IGF-II triggers IGF-IIR receptor activation, causing mitochondria dysfunction, resulting in mitophagy, and cardiomyocyte cell death...
March 25, 2018: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29531824/nr4a2-protects-cardiomyocytes-against-myocardial-infarction-injury-by-promoting-autophagy
#11
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
https://www.readbyqxmd.com/read/29526917/-the-critical-role-of-autophagy-in-heart-failure
#12
Yasuhiro Maejima
Autophagy is an evolutionarily conserved process for degradation of long-lived proteins and organelles that govern a number of cardiac pathologies which cause heart failure. Indeed, recent investigations have uncovered pathways that regulate autophagy in the heart and underlying mechanisms by which alterations in this process affect cardiac function and structure. One of the major roles of autophagy in cardiomyocytes is the intracellular protein quality control (PQC). Impairment of autophagy causes aggregation of damaged and/or misfolded proteins in cardiomyocytes, thereby damaging the cells which, in turn leads to pathological cardiac remodeling...
2018: Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
https://www.readbyqxmd.com/read/29521549/cardiac-adenovirus-associated-viral-presenilin-1-gene-delivery-protects-the-left-ventricular-function-of-the-heart-via-regulating-ryr2-function-in-post-ischaemic-heart-failure
#13
Tian Li, Yafeng Shen, Li Su, Xiaoyan Fan, Fangxing Lin, Xuting Ye, Dianer Ding, Ying Tang, Yongji Yang, Changhai Lei, Shi Hu
Post-ischaemic 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 ischaemia/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-ischaemic heart failure...
March 21, 2018: Journal of Drug Targeting
https://www.readbyqxmd.com/read/29519677/autophagic-control-of-cardiac-steatosis-through-fgf21-in-obesity-associated-cardiomyopathy
#14
C Rupérez, C Lerin, G Ferrer-Curriu, M Cairo, A Mas-Stachurska, M Sitges, J Villarroya, M Giralt, F Villarroya, A Planavila
OBJECTIVE: High-fat diet-induced obesity leads to the development of hypertrophy and heart failure through poorly understood molecular mechanisms. We have recently shown that fibroblast growth factor-21 (FGF21) is produced by the heart and exerts protective effects that prevent cardiac hypertrophy development and oxidative stress. The aim of this study was to determine the effects of FGF21 on the cardiomyopathy associated with obesity development. RESULTS: Fgf21-/- mice showed an enhanced increase in the heart weight/tibia length (HW/TL) ratio in response to the high-fat diet...
June 1, 2018: International Journal of Cardiology
https://www.readbyqxmd.com/read/29501491/blockage-of-akap12-accelerates-angiotensin-ii-ang-ii-induced-cardiac-injury-in-mice-by-regulating-the-transforming-growth-factor-%C3%AE-1-tgf-%C3%AE-1-pathway
#15
Yong Li, Qiu-Hua Yu, Ying Chu, Wei-Min Wu, Jian-Xiang Song, Xiao-Bo Zhu, Qiang Wang
Hypertension is a multifactorial chronic inflammatory disease that leads to cardiac remodeling. A-kinase anchor protein 12 (AKAP12) is a scaffolding protein that has multiple functions in various biological events, including the regulation of vessel integrity and differentiation of neural barriers in blood. However, the role of AKAP12 in angiotensin II (Ang II)-induced cardiac injury remains unclear. In the present study, Ang II infusion reduced AKAP12 expressions in the hearts of wild-type (WT) mice, and AKAP12 knockout (KO) enhanced the infiltration of inflammatory cells...
May 5, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29446053/systems-pharmacological-analysis-of-mitochondrial-cardiotoxicity-induced-by-selected-tyrosine-kinase-inhibitors
#16
Tanaya Vaidya, Jeff Kamta, Maher Chaar, Anusha Ande, Sihem Ait-Oudhia
Tyrosine kinase inhibitors (TKIs) are targeted therapies rapidly becoming favored over conventional cytotoxic chemotherapeutics. Our study investigates two FDA approved TKIs, DASATINIB; indicated for IMATINIB-refractory chronic myeloid leukemia, and SORAFENIB; indicated for hepatocellular carcinoma and advanced renal cell carcinoma. Limited but crucial evidence suggests that these agents can have cardiotoxic side effects ranging from hypertension to heart failure. A greater understanding of the underlying mechanisms of this cardiotoxicity are needed as concerns grow and the capacity to anticipate them is lacking...
February 14, 2018: Journal of Pharmacokinetics and Pharmacodynamics
https://www.readbyqxmd.com/read/29420210/new-insights-into-the-role-of-mtor-signaling-in-the-cardiovascular-system
#17
REVIEW
Sebastiano Sciarretta, Maurizio Forte, Giacomo Frati, Junichi Sadoshima
The mTOR (mechanistic target of rapamycin) is a master regulator of several crucial cellular processes, including protein synthesis, cellular growth, proliferation, autophagy, lysosomal function, and cell metabolism. mTOR interacts with specific adaptor proteins to form 2 multiprotein complexes, called mTORC1 (mTOR complex 1) and mTORC2 (mTOR complex 2). In the cardiovascular system, the mTOR pathway regulates both physiological and pathological processes in the heart. It is needed for embryonic cardiovascular development and for maintaining cardiac homeostasis in postnatal life...
February 2, 2018: Circulation Research
https://www.readbyqxmd.com/read/29351515/understanding-key-mechanisms-of-exercise-induced-cardiac-protection-to-mitigate-disease-current-knowledge-and-emerging-concepts
#18
Bianca C Bernardo, Jenny Y Y Ooi, Kate L Weeks, Natalie L Patterson, Julie R McMullen
The benefits of exercise on the heart are well recognized, and clinical studies have demonstrated that exercise is an intervention that can improve cardiac function in heart failure patients. This has led to significant research into understanding the key mechanisms responsible for exercise-induced cardiac protection. Here, we summarize molecular mechanisms that regulate exercise-induced cardiac myocyte growth and proliferation. We discuss in detail the effects of exercise on other cardiac cells, organelles, and systems that have received less or little attention and require further investigation...
January 1, 2018: Physiological Reviews
https://www.readbyqxmd.com/read/29331057/manifestations-and-mechanisms-of-myocardial-lipotoxicity-in-obesity
#19
A C Sletten, L R Peterson, J E Schaffer
Environmental and socioeconomic changes over the past thirty years have contributed to a dramatic rise in the worldwide prevalence of obesity. Heart disease is amongst the most serious health risks of obesity, with increases in both atherosclerotic coronary heart disease and heart failure among obese individuals. In this review, we focus on primary myocardial alterations in obesity that include hypertrophic remodelling and diastolic dysfunction. Obesity-associated perturbations in myocardial and systemic lipid metabolism are important contributors to cardiovascular complications of obesity...
January 13, 2018: Journal of Internal Medicine
https://www.readbyqxmd.com/read/29323723/haplo-insufficiency-of-bcl2-associated-athanogene-3-in-mice-results-in-progressive-left-ventricular-dysfunction-%C3%AE-adrenergic-insensitivity-and-increased-apoptosis
#20
Valerie D Myers, Dhanendra Tomar, Muniswamy Madesh, JuFang Wang, Jianliang Song, Xue-Qian Zhang, Manish K Gupta, Farzaneh G Tahrir, Jennifer Gordon, Joseph M McClung, Christopher D Kontos, Kamel Khalili, Joseph Y Cheung, Arthur M Feldman
Bcl2-associated athanogene 3 (BAG3) is a 575 amino acid protein that is found predominantly in the heart, skeletal muscle, and many cancers. Deletions and truncations in BAG3 that result in haplo-insufficiency have been associated with the development of dilated cardiomyopathy. To study the cellular and molecular events attributable to BAG3 haplo-insufficiency we generated a mouse in which one allele of BAG3 was flanked by loxP recombination sites (BAG3fl/+ ). Mice were crossed with α-MHC-Cre mice in order to generate mice with cardiac-specific haplo-insufficiency (cBAG3+/-) and underwent bi-weekly echocardiography to assess their cardiac phenotype...
January 11, 2018: Journal of Cellular Physiology
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