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JOURNAL ARTICLE
Jing-Yi Dang, Wei Zhang, Yi Chu, Jiang-Hong Chen, Zhao-Le Ji, Pin Feng
INTRODUCTION: Salusins, which are translated from the alternatively spliced mRNA of torsin family 2 member A (TOR2A), play a vital role in regulation of various cardiovascular diseases. However, it remains unclear precisely regarding their roles in hypertrophic cardiomyopathy (HCM). Therefore, this study was conducted to explore therapeutic effect and the underlying mechanisms of salusins on HCM. MATERIAL AND METHODS: In vivo experiments, Sprague-Dawley rats were used to induce HCM model by angiotensin (Ang) II infusion for 4 weeks...
February 9, 2024: European Journal of Medical Research
#2
JOURNAL ARTICLE
Rongjun Zou, Wanting Shi, Asli F Ceylan, Maolong Dong, Miao Zhang, Zengxiao Zou, Bo Peng, Feng Dong, Subat Turdi, Jie Lin, Yingmei Zhang, Ge Wang, Xiaoping Fan, Jun Ren
Advanced aging evokes unfavorable changes in the heart including cardiac remodeling and contractile dysfunction although the underlying mechanism remains elusive. This study was conducted to evaluate the role of endothelin-1 (ET-1) in the pathogenesis of cardiac aging and mechanism involved. Echocardiographic and cardiomyocyte mechanical properties were determined in young (5-6 mo) and aged (26-28 mo) wild-type (WT) and cardiomyocyte-specific ETA receptor knockout (ETA KO) mice. GSEA enrichment identified differentially expressed genes associated with mitochondrial respiration, mitochondrial protein processing and mitochondrial depolarization in cardiac aging...
November 12, 2023: Biochimica et Biophysica Acta. Molecular Basis of Disease
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JOURNAL ARTICLE
Anbo Gao, Mengjie Wang, Xing Tang, Gangqing Shi, Kai Hou, Jinren Fang, Linlin Zhou, Hong Zhou, Weimin Jiang, Yukun Li, Fan Ouyang
Radiation-induced heart damage caused by low-dose X-rays has a significant impact on tumour patients' prognosis, with cardiac hypertrophy being the most severe noncarcinogenic adverse effect. Our previous study demonstrated that mitophagy activation promoted cardiac hypertrophy, but the underlying mechanisms remained unclear. In the present study, PARL-IN-1 enhanced excessive hypertrophy of cardiomyocytes and exacerbated mitochondrial damage. Isobaric tags for relative and absolute quantification-based quantitative proteomics identified NDP52 as a crucial target mediating cardiac hypertrophy induced by low-dose X-rays...
November 9, 2023: Journal of Cellular Physiology
#4
JOURNAL ARTICLE
Moritz Borger, Clarissa von Haefen, Christoph Bührer, Stefanie Endesfelder
Preterm birth is a risk factor for cardiometabolic disease. The preterm heart before terminal differentiation is in a phase that is crucial for the number and structure of cardiomyocytes in further development, with adverse effects of hypoxic and hyperoxic events. Pharmacological intervention could attenuate the negative effects of oxygen. Dexmedetomidine (DEX) is an α2-adrenoceptor agonist and has been mentioned in connection with cardio-protective benefits. In this study, H9c2 myocytes and primary fetal rat cardiomyocytes (NRCM) were cultured for 24 h under hypoxic condition (5% O2 ), corresponding to fetal physioxia (pO2 32-45 mmHg), ambient oxygen (21% O2 , pO2 ~150 mmHg), or hyperoxic conditions (80% O2 , pO2 ~300 mmHg)...
June 2, 2023: Antioxidants (Basel, Switzerland)
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JOURNAL ARTICLE
Lin Hu, Ziyuan Wang, Huan Li, Jiarui Wei, Fengyue Tang, Qing Wang, Jing Wang, Xiaoqiao Zhang, Qiufang Zhang
Icariin (ICA), a bioactive flavonoid compound derived from Epimedium, have been demonstrated possessing anti-oxidative stress, anti-inflammation in the cardiovascular disease. But its effects on cardiomyocyte hypertrophy and the underlying mechanisms remains unclear. Here we found that ICA alleviated ISO-induced H9c2 or NRCM myocytes hypertrophy, assessed by surface area and the expression of ANP, BNP and β-MHC. Furthemore, ICA reversed cardiomcytes enlargment by suppresing apoptotic injury and increasing autophagic flux...
February 19, 2022: Biochemical and Biophysical Research Communications
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JOURNAL ARTICLE
Jihoon Nah, Akihiro Shirakabe, Risa Mukai, Peiyong Zhai, Eun-Ah Sung, Andreas Ivessa, Wataru Mizushima, Yasuki Nakada, Toshiro Saito, Chengchen Hu, Yong-Keun Jung, Junichi Sadoshima
AIMS: Well-controlled mitochondrial homeostasis, including a mitochondria-specific form of autophagy (hereafter referred to as mitophagy), is essential for maintaining cardiac function. The molecular mechanism mediating mitophagy during PO is poorly understood. We have shown previously that mitophagy in the heart is mediated primarily by Atg5/Atg7-independent mechanisms, including Unc-51-like kinase1 (Ulk1)-dependent alternative mitophagy, during myocardial ischemia. Here, we investigated the role of alternative mitophagy in the heart during PO-induced hypertrophy...
January 9, 2022: Cardiovascular Research
#7
JOURNAL ARTICLE
Tongtong Shen, Yu Liu, Shuangshuang Dong, Xiaohong Xu, Xinxin Wang, Yong Li, Limin Zhou
Alarin could alleviate myocardial infarction-induced heart failure. The present study was to explore whether alarin could alleviate myocardial hypertrophy via inhibiting cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signaling pathway to attenuate autophagy. Myocardial hypertrophy was induced by angiotensin (Ang) II infusion in vivo in mice and by Ang II treatment of neonatal rat cardiomyocytes (NRCMs) in vitro. The Ang II-induced hypertrophy and fibrosis of the heart were alleviated after alarin administration in mice...
October 5, 2021: Peptides
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JOURNAL ARTICLE
Christiane Ott, Tobias Jung, Sarah Brix, Cathleen John, Iris R Betz, Anna Foryst-Ludwig, Stefanie Deubel, Wolfgang M Kuebler, Tilman Grune, Ulrich Kintscher, Jana Grune
Cardiac remodeling and contractile dysfunction are leading causes in hypertrophy-associated heart failure (HF), increasing with a population's rising age. A hallmark of aged and diseased hearts is the accumulation of modified proteins caused by an impaired autophagy-lysosomal-pathway. Although, autophagy inducer rapamycin has been described to exert cardioprotective effects, it remains to be shown whether these effects can be attributed to improved cardiomyocyte autophagy and contractility. In vivo hypertrophy was induced by transverse aortic constriction (TAC), with mice receiving daily rapamycin injections beginning six weeks after surgery for four weeks...
April 4, 2021: Cells
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JOURNAL ARTICLE
Mingjun Shi, Sierra Shepard, Zhiyong Zhou, Jenny Maique, Olivia Seli, Orson W Moe, Ming Chang Hu
High phosphate contributes to uremic cardiomyopathy. Abnormal autophagy is associated with the development and progression of heart disease. What is unknown is the effects of phosphate on autophagy and whether the ill effects of phosphate on cardiomyocytes are mediated by low autophagy. High (2.0% w / w )-phosphate diet reduced LC3 puncta in cardiomyocytes and ratio of LC3 II/I and increased p62 protein, indicating that autophagy activity was suppressed. Mice with cardiomyocyte-specific deletion of autophagy-related protein 5 ( H-atg5 -/- ) had reduced autophagy only in the heart, developed cardiac dysfunction with hypertrophy and fibrosis, and had a short lifespan...
April 1, 2021: Cells
#10
JOURNAL ARTICLE
Senka Ljubojević-Holzer, Simon Kraler, Nataša Djalinac, Mahmoud Abdellatif, Julia Voglhuber, Julia Schipke, Marlene Schmidt, Katharina-Maria Kling, Greta Therese Franke, Viktoria Herbst, Andreas Zirlik, Dirk von Lewinski, Daniel Scherr, Peter P Rainer, Michael Kohlhaas, Alexander Nickel, Christian Mühlfeld, Christoph Maack, Simon Sedej
AIMS: Autophagy protects against the development of cardiac hypertrophy and failure. While aberrant Ca2+ handling promotes myocardial remodelling and contributes to contractile dysfunction, the role of autophagy in maintaining Ca2+ homeostasis remains elusive. Here, we examined whether Atg5 deficiency-mediated autophagy promotes early changes in subcellular Ca2+ handling in ventricular cardiomyocytes, and whether those alterations associate with compromised cardiac reserve capacity, which commonly precedes the onset of heart failure...
March 22, 2021: Cardiovascular Research
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JOURNAL ARTICLE
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
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JOURNAL ARTICLE
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
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JOURNAL ARTICLE
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
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JOURNAL ARTICLE
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
#15
JOURNAL ARTICLE
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
#16
JOURNAL ARTICLE
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
#17
JOURNAL ARTICLE
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
#18
JOURNAL ARTICLE
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
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JOURNAL ARTICLE
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
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JOURNAL ARTICLE
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
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