Why the study?
Pathological changes in the microtubule network organization increase cellular stiffness and cause contractile dysfunction, prompting a review of the role and mechanisms of microtubules in heart failure.
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Design
Narrative review of literature published from 2012 to 2022
MTN changes may drive HF stiffness; hypothesis-generating and requires validation before any therapeutic targeting.
Heart failure (HF) is a complex pathological state in which cardiac performance fails to match perfusion demand, commonly preceded by an enlargement of the heart known as cardiac hypertrophy. Pathological changes in the microtubule network (MTN) organization have been shown to increase cellular stiffness and lead to contractile dysfunction of cardiomyocytes. In this narrative review, we are focusing on the role of the microtubule and also its mechanism in the heart, especially in HF. We conducted literature research for published articles carried out from 2012 to 2022. Microtubules are polymers that serve as structural elements with the shape of long, rigid tubes that are highly dynamic. The stiffness of the myocardium is largely influenced by the MTN. Through various methods, the MTN is remodeled during cardiac hypertrophy and HF. Targeting microtubules for the treatment of HF might become a new approach to improve the outcome. While colchicine inhibits various microtubule-dependent cellular in interphase cells and proliferation, it needs further study for the safety of the adjusted dosage. Manipulating detyrosination of microtubules might be useful for restoring the function of failing myocytes although there are still very limited data on this.
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Purwowiyoto et al. (2023) studied this question.
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