Abstract
The incidence and prevalence of cardiac diseases, which are the main cause of death worldwide, are likely to increase because of population ageing and changes in lifestyle. Prevailing theories about the mechanisms of cardiac disease onset feature the gradual derailment of cellular protein homeostasis (proteostasis) and loss of the protein quality control as central factors. In the heart, loss of protein patency, due to flaws in design (genetically) or environmentally-induced wear and tear, may overwhelm protein quality control, thereby triggering derailment of proteostasis and contributing to cardiac disease onset.
Highlights
The contribution of Dorsch is directed at identification of key players within the protein quality control system to underlie hypertrophic cardiomyopathy [2]
They observed, in human heart tissue of patients carrying a mutation in sarcomeric proteins, increased levels of heat shock proteins (HSP) and acetylated α-tubulin compared to mutation negative patients
As acetylated tubulin results in polymerization of microtubules and stabilization of cardiomyocyte structure, the findings suggest a role for HSP in microtubular network proliferation to compensate for sarcomeric loss in mutation-induced hypertrophic cardiomyopathy
Summary
The contribution of Dorsch is directed at identification of key players within the protein quality control system to underlie hypertrophic cardiomyopathy [2]. As acetylated tubulin results in polymerization of microtubules and stabilization of cardiomyocyte structure, the findings suggest a role for HSP in microtubular network proliferation to compensate for sarcomeric loss in mutation-induced hypertrophic cardiomyopathy. In line with these findings, Singh elaborates on the role of the intermediate filament protein desmin in cardiac function [3]. These may hamper cardiomyocyte function and lead to cardiac disease onset.
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