Mechanisms contributing to cardiac remodelling
Qing-Qing Wu1,2,3, Yang Xiao1,2,3, Yuan Yuan1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Insights
Pathological cardiac remodelling involves detrimental changes in the heart
Area of Science:
- Cardiovascular biology and pathology
Background:
- Cardiac remodelling is adaptive (physiological) or maladaptive (pathological).
- Pathological cardiac remodelling precedes clinical heart failure (HF).
Purpose of the Study:
- To review the molecular and cellular mechanisms driving pathological cardiac remodelling.
Main Methods:
- Literature review of molecular and cellular responses in pathological cardiac remodelling.
Main Results:
- Pathological remodelling involves fibrosis, inflammation, and cellular dysfunction.
- Key cellular dysfunctions include altered cardiomyocyte interactions, oxidative stress, ER stress, and metabolic impairment.
Conclusions:
- Understanding these molecular and cellular pathways is crucial for developing therapies for heart failure.
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.
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