| Literature DB >> 28842527 |
Qing-Qing Wu1,2,3, Yang Xiao1,2,3, Yuan Yuan1,2,3, Zhen-Guo Ma1,2,3, Hai-Han Liao1,2,3, Chen Liu1,2,3, Jin-Xiu Zhu1,2,3, Zheng Yang1,2,3, Wei Deng1,2,3, Qi-Zhu Tang4,2,3.
Abstract
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.Entities:
Keywords: cardiac remodelling; cardiomyocytes; heart failure; noncardiomyocytes; signalling
Mesh:
Year: 2017 PMID: 28842527 DOI: 10.1042/CS20171167
Source DB: PubMed Journal: Clin Sci (Lond) ISSN: 0143-5221 Impact factor: 6.124