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). Pathological remodelling is associated with fibrosis, inflammation and cellular dysfunction (e.g. abnormal cardiomyocyte/non-cardiomyocyte interactions, oxidative stress, endoplasmic reticulum (ER) stress, autophagy alterations, impairment of metabolism and signalling pathways), leading to HF. This review describes the key molecular and cellular responses involved in pathological cardiac remodelling.
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A flurogold labeled-retina flatmount (front) representing surviving retinal ganglion cells, and the chemical structure of trimetazidine (background). In Clinical Science volume 131, issue 18, Wan et al. report that trimetazidine protects retinal ganglion cells against acute glaucoma via the Nrf2/Ho-1 pathway and propose it as a novel therapeutic agent; for details, see pages 2363-2375.
Review Article|
August 25 2017
Mechanisms contributing to cardiac remodelling
Qing-Qing Wu;
Qing-Qing Wu
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Yang Xiao;
Yang Xiao
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Yuan Yuan;
Yuan Yuan
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Zhen-Guo Ma;
Zhen-Guo Ma
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Hai-Han Liao;
Hai-Han Liao
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Chen Liu;
Chen Liu
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Jin-Xiu Zhu;
Jin-Xiu Zhu
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Zheng Yang;
Zheng Yang
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Wei Deng;
Wei Deng
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
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Qi-zhu Tang
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China
2Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China
3Hubei Key Laboratory of Cardiology, Department of Cardiology, Renmin Hospital of Wuhan University,Wuhan 430060, P.R. China
Correspondence: Qi-zhu Tang ([email protected])
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Publisher: Portland Press Ltd
Received:
June 23 2017
Revision Received:
July 26 2017
Accepted:
July 31 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2017
Clin Sci (Lond) (2017) 131 (18): 2319–2345.
Article history
Received:
June 23 2017
Revision Received:
July 26 2017
Accepted:
July 31 2017
Citation
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; Mechanisms contributing to cardiac remodelling. Clin Sci (Lond) 15 September 2017; 131 (18): 2319–2345. doi: https://doi.org/10.1042/CS20171167
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