Key result
Molecular biomarkers including micro-RNAs, VEGF-B, SIRT3, GDF15, and glycoprotein 130 play important roles in the development and progression of myocardial hypertrophy.
Why the study?
Heart dysfunction is often associated with myocardial remodelling caused by cardiac hypertrophy, prompting a need to understand the potential molecular mechanisms involved in its development and progression.
Understanding the regulatory mechanisms of micro-RNAs and other molecular biomarkers in the heart may help identify new molecular targets for the treatment of cardiac hypertrophy.
Answers are grounded in this paper and cite their sources.
May guide future hypertrophy therapies; leaves open clinical validation of these biomarkers.
Cardiac hypertrophy is characterized by an increase in myocyte size in the absence of cell division. This condition is thought to be an adaptive response to cardiac wall stress resulting from the enhanced cardiac afterload. The pathogenesis of heart dysfunction, which is one of the primary causes of morbidity and mortality in elderly people, is often associated with myocardial remodelling caused by cardiac hypertrophy. In order to well understand the potential mechanisms, we described the molecules involved in the development and progression of myocardial hypertrophy. Increasing evidence has indicated that micro-RNAs are involved in the pathogenesis of cardiac hypertrophy. In addition, molecular biomarkers including vascular endothelial growth factor B, NAD-dependent deacetylase sirtuin-3, growth/differentiation factor 15 and glycoprotein 130, also play important roles in the development of myocardial hypertrophy. Knowing the regulatory mechanisms of these biomarkers in the heart may help identify new molecular targets for the treatment of cardiac hypertrophy.
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Liu et al. (2019) conducted a review in Cardiac hypertrophy. Molecular biomarkers was evaluated. Molecular biomarkers including micro-RNAs, VEGF-B, SIRT3, GDF15, and glycoprotein 130 play important roles in the development and progression of myocardial hypertrophy.
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