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ATG5 and cardiomyocyte hypertrophy

Wenbin Gao, Zheng Zhou, Birong Liang, Yusheng Huang, Zhongqi Yang, Yang Chen, Lu Zhang, Cui Yan, Jiajia Wang, Lu Lu, Zhaorui Wen, Shaoxiang Xian, Lingjun Wang
The receptor for advanced glycation end products (RAGE) is involved in heart failure (HF) by mediating diverse pathologic processes, including the promotion of inflammation and autophagy. However, the role of RAGE in pressure overload-induced HF is not well understood. We found that stimulation of RAGE triggered the death of neonatal rat ventricular myocytes (NRVMs), while cell death was alleviated by ATG5 knockdown. Using transverse aortic constriction (TAC) in mice as a model of pressure overload-induced HF, we demonstrated that RAGE knockout or RAGE blockade attenuated cardiac hypertrophy and fibrosis as well as cardiac dysfunction at 8 weeks after TAC...
2018: Frontiers in Physiology
Yong-Zeng Chen, Fan Wang, Hai-Jun Wang, Hong-Bin Liu
Objective: To investigate the role of sphingosine-1-phosphate (S1P) and its receptors in cardiomyocyte autophagy, cardiomyocyte hypertrophy and cardiac function. Methods: Cardiomyocytes were isolated from neonatal Vista rats. Autophagy and hypertrophy of cardiomyocytes were induced via starvation culture and phenylephrine (PE), respectively, and S1P was used to treat the cardiomyocytes. The effect of S1P on cardiomyocyte autophagy was evaluated by the number of autophagosomes, the expression of autophagy-related proteins and autophagic marker genes in cardiomyocytes...
May 2018: Journal of Geriatric Cardiology: JGC
Ru-Li Li, Si-Si Wu, Yao Wu, Xiao-Xiao Wang, Hong-Ying Chen, Juan-Juan Xin, He Li, Jie Lan, Kun-Yue Xue, Xue Li, Cai-Li Zhuo, Yu-Yan Cai, Jin-Han He, Heng-Yu Zhang, Chao-Shu Tang, Wang Wang, Wei Jiang
In hypertrophic hearts, autophagic flux insufficiency is recognized as a key pathology leading to maladaptive cardiac remodeling and heart failure. This study aimed to illuminate the cardioprotective role and mechanisms of a new myokine and adipokine, irisin, in cardiac hypertrophy and remodeling. Adult male wild-type, mouse-FNDC5 (irisin-precursor)-knockout and FNDC5 transgenic mice received 4 weeks of transverse aortic constriction (TAC) alone or combined with intraperitoneal injection of chloroquine diphosphate (CQ)...
August 2018: Journal of Molecular and Cellular Cardiology
Jia-Pu Wang, Rui-Fang Chi, Ke Wang, Teng Ma, Xiao-Fei Guo, Xiao-Li Zhang, Bao Li, Fu-Zhong Qin, Xue-Bin Han, Bian-Ai Fan
NEW FINDINGS: What is the central question of this study? Does oxidative stress induce impairment of autophagy that results in myocyte hypertrophy early after pressure overload? What is the main finding and its importance? In cultured myocytes, hydrogen peroxide decreased autophagy and increased hypertrophy, and inhibition of autophagy enhanced myocyte hypertrophy. In rats with early myocardial hypertrophy after pressure overload, myocyte autophagy was progressively decreased. The antioxidant N-acetyl-cysteine or the superoxide dismutase mimic tempol prevented the decrease of myocyte autophagy and attenuated myocyte hypertrophy early after pressure overload...
April 1, 2018: Experimental Physiology
Tobias Eisenberg, Mahmoud Abdellatif, Sabrina Schroeder, Uwe Primessnig, Slaven Stekovic, Tobias Pendl, Alexandra Harger, Julia Schipke, Andreas Zimmermann, Albrecht Schmidt, Mingming Tong, Christoph Ruckenstuhl, Christopher Dammbrueck, Angelina S Gross, Viktoria Herbst, Christoph Magnes, Gert Trausinger, Sophie Narath, Andreas Meinitzer, Zehan Hu, Alexander Kirsch, Kathrin Eller, Didac Carmona-Gutierrez, Sabrina Büttner, Federico Pietrocola, Oskar Knittelfelder, Emilie Schrepfer, Patrick Rockenfeller, Corinna Simonini, Alexandros Rahn, Marion Horsch, Kristin Moreth, Johannes Beckers, Helmut Fuchs, Valerie Gailus-Durner, Frauke Neff, Dirk Janik, Birgit Rathkolb, Jan Rozman, Martin Hrabe de Angelis, Tarek Moustafa, Guenter Haemmerle, Manuel Mayr, Peter Willeit, Marion von Frieling-Salewsky, Burkert Pieske, Luca Scorrano, Thomas Pieber, Raimund Pechlaner, Johann Willeit, Stephan J Sigrist, Wolfgang A Linke, Christian Mühlfeld, Junichi Sadoshima, Joern Dengjel, Stefan Kiechl, Guido Kroemer, Simon Sedej, Frank Madeo
Aging is associated with an increased risk of cardiovascular disease and death. Here we show that oral supplementation of the natural polyamine spermidine extends the lifespan of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial respiration, and it also improved the mechano-elastical properties of cardiomyocytes in vivo, coinciding with increased titin phosphorylation and suppressed subclinical inflammation...
December 2016: Nature Medicine
Sheng Xie, Yan Deng, Yue-Ying Pan, Jie Ren, Meng Jin, Yu Wang, Zhi-Hua Wang, Die Zhu, Xue-Ling Guo, Xiao Yuan, Jin Shang, Hui-Guo Liu
Autophagy is tightly regulated to maintain cardiac homeostasis. Impaired autophagy is closely associated with pathological cardiac hypertrophy. However, the relationship between autophagy and cardiac hypertrophy induced by chronic intermittent hypoxia (CIH) is not known. In the present study, we measured autophagy-related genes and autophagosomes during 10 weeks of CIH in rats, and 6 days in H9C2 cardiomyocytes, and showed that autophagy was impaired. This conclusion was confirmed by the autophagy flux assay...
September 15, 2016: Archives of Biochemistry and Biophysics
Z Li, Y Song, L Liu, N Hou, X An, D Zhan, Y Li, L Zhou, P Li, L Yu, J Xia, Y Zhang, J Wang, X Yang
Basal autophagy is tightly regulated by transcriptional and epigenetic factors to maintain cellular homeostasis. Dysregulation of cardiac autophagy is associated with heart diseases, including cardiac hypertrophy, but the mechanism governing cardiac autophagy is rarely identified. To analyze the in vivo function of miR-199a in cardiac autophagy and cardiac hypertrophy, we generated cardiac-specific miR-199a transgenic mice and showed that overexpression of miR-199a was sufficient to inhibit cardiomyocyte autophagy and induce cardiac hypertrophy in vivo...
July 2017: Cell Death and Differentiation
Anne-Coline Laurent, Malik Bisserier, Alexandre Lucas, Florence Tortosa, Marie Roumieux, Annélie De Régibus, Audrey Swiader, Yannis Sainte-Marie, Christophe Heymes, Cécile Vindis, Frank Lezoualc'h
AIMS: Stimulation of β-adrenergic receptors (β-AR) increases cAMP production and contributes to the pathogenesis of cardiac hypertrophy and failure through poorly understood mechanisms. We previously demonstrated that Exchange protein directly activated by cAMP 1 (Epac1)-induced hypertrophy in primary cardiomyocytes. Among the mechanisms triggered by cardiac stress, autophagy has been highlighted as a protective or harmful response. Here, we investigate whether Epac1 promotes cardiac autophagy and how altered autophagy has an impact on Epac1-induced cardiomyocyte hypertrophy...
January 1, 2015: Cardiovascular Research
Li-qing Weng, Wen-bin Zhang, Yong Ye, Pei-pei Yin, Jie Yuan, Xing-xu Wang, Le Kang, Sha-sha Jiang, Jie-yun You, Jian Wu, Hui Gong, Jun-bo Ge, Yun-zeng Zou
AIM: Aliskiren (ALK) is a renin inhibitor that has been used in the treatment of hypertension. The aim of this study was to determine whether ALK could ameliorate pressure overload-induced heart hypertrophy and fibrosis, and to elucidate the mechanisms of action. METHODS: Transverse aortic constriction (TAC) was performed in mice to induce heart pressure overload. ALK (150 mg·kg(-1)·d(-1), po), the autophagy inhibitor 3-methyladenine (10 mg·kg(-1) per week, ip) or the PKCβI inhibitor LY333531 (1 mg·kg(-1)·d-(1), po) was administered to the mice for 4 weeks...
August 2014: Acta Pharmacologica Sinica
Asli F Ceylan-Isik, Maolong Dong, Yingmei Zhang, Feng Dong, Subat Turdi, Sreejayan Nair, Masashi Yanagisawa, Jun Ren
Cardiac aging is manifested as cardiac remodeling and contractile dysfunction although precise mechanisms remain elusive. This study was designed to examine the role of endothelin-1 (ET-1) in aging-associated myocardial morphological and contractile defects. Echocardiographic and cardiomyocyte contractile properties were evaluated in young (5-6 months) and old (26-28 months) C57BL/6 wild-type and cardiomyocyte-specific ET(A) receptor knockout (ETAKO) mice. Cardiac ROS production and histology were examined...
March 2013: Basic Research in Cardiology
Yinan Hua, Yingmei Zhang, Asli F Ceylan-Isik, Loren E Wold, Jennifer M Nunn, Jun Ren
Aging is often accompanied with geometric and functional changes in the heart, although the underlying mechanisms remain unclear. Recent evidence has described a potential role of Akt and autophagy in aging-associated organ deterioration. This study was to examine the impact of cardiac-specific Akt activation on aging-induced cardiac geometric and functional changes and underlying mechanisms involved. Cardiac geometry, contractile and intracellular Ca(2+) properties were evaluated using echocardiography, edge-detection and fura-2 techniques...
November 2011: Basic Research in Cardiology
Dian J Cao, Zhao V Wang, Pavan K Battiprolu, Nan Jiang, Cyndi R Morales, Yongli Kong, Beverly A Rothermel, Thomas G Gillette, Joseph A Hill
Histone deacetylases (HDACs) regulate cardiac plasticity; however, their molecular targets are unknown. As autophagy contributes to pathological cardiac remodeling, we hypothesized that HDAC inhibitors target autophagy. The prototypical HDAC inhibitor (HDACi), trichostatin A (TSA), attenuated both load- and agonist-induced hypertrophic growth and abolished the associated activation of autophagy. Phenylephrine (PE)-triggered hypertrophy and autophagy in cultured cardiomyocytes were each blocked by a panel of structurally distinct HDAC inhibitors...
March 8, 2011: Proceedings of the National Academy of Sciences of the United States of America
Atsuko Nakai, Osamu Yamaguchi, Toshihiro Takeda, Yoshiharu Higuchi, Shungo Hikoso, Masayuki Taniike, Shigemiki Omiya, Isamu Mizote, Yasushi Matsumura, Michio Asahi, Kazuhiko Nishida, Masatsugu Hori, Noboru Mizushima, Kinya Otsu
Autophagy, an evolutionarily conserved process for the bulk degradation of cytoplasmic components, serves as a cell survival mechanism in starving cells. Although altered autophagy has been observed in various heart diseases, including cardiac hypertrophy and heart failure, it remains unclear whether autophagy plays a beneficial or detrimental role in the heart. Here, we report that the cardiac-specific loss of autophagy causes cardiomyopathy in mice. In adult mice, temporally controlled cardiac-specific deficiency of Atg5 (autophagy-related 5), a protein required for autophagy, led to cardiac hypertrophy, left ventricular dilatation and contractile dysfunction, accompanied by increased levels of ubiquitination...
May 2007: Nature Medicine
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