Key result
Modified cardiomyocyte microtubules proliferate in cardiovascular disease to impede contractility and drive cardiac dysfunction.
Why the study?
Recent studies have revealed new canonical and noncanonical roles of cardiomyocyte microtubules in regulating mechanics, transport, and contractile dysfunction.
Cardiomyocyte microtubules play essential roles in mechanics and transport, and their disease-associated proliferation contributes to contractile dysfunction.
Microtubule proliferation may contribute to contractile dysfunction in CVD; leaves open targeted therapies pending interventional studies.
Microtubules are essential cytoskeletal elements found in all eukaryotic cells. The structure and composition of microtubules regulate their function, and the dynamic remodeling of the network by posttranslational modifications and microtubule-associated proteins generates diverse populations of microtubules adapted for various contexts. In the cardiomyocyte, the microtubules must accommodate the unique challenges faced by a highly contractile, rigidly structured, and long-lasting cell. Through their canonical trafficking role and positioning of mRNA, proteins, and organelles, microtubules regulate essential cardiomyocyte functions such as electrical activity, calcium handling, protein translation, and growth. In a more specialized role, posttranslationally modified microtubules form load-bearing structures that regulate myocyte mechanics and mechanotransduction. Modified microtubules proliferate in cardiovascular diseases, creating stabilized resistive elements that impede cardiomyocyte contractility and contribute to contractile dysfunction. In this review, we highlight the most exciting new concepts emerging from recent studies into canonical and noncanonical roles of cardiomyocyte microtubules.
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Uchida et al. (2021) conducted a review in Cardiovascular diseases. Cardiomyocyte microtubules regulate essential cellular functions and mechanics, with modified microtubules proliferating in cardiovascular diseases to impede contractility and contribute to dysfunction.
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