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Cardiac regeneration and remodelling of the cardiomyocyte cytoarchitecture.

07:00 EST 19th November 2019 | BioPortfolio

Summary of "Cardiac regeneration and remodelling of the cardiomyocyte cytoarchitecture."

Adult mammals are unable to regenerate their hearts after cardiac injury; largely due to the incapacity of cardiomyocytes to undergo cell division. However, mammalian embryonic and foetal cardiomyocytes, similar to cardiomyocytes from fish and amphibians during their entire life, exhibit robust replicative activity, which stops abruptly after birth and never significantly resumes. Converging evidence indicates that formation of the highly ordered and stable cytoarchitecture of mammalian mature cardiomyocytes is coupled with loss of their proliferative potential. Here, we review the available information on the role of the cardiac cytoskeleton and sarcomere in the regulation of cardiomyocyte proliferation. The actin cytoskeleton, the intercalated disc, the microtubular network and the dystrophin glycoprotein complex each sense mechanical cues from the surrounding environment. Furthermore, they participate in the regulation of cardiomyocyte proliferation by impinging on the YAP/TAZ, β-catenin and MRTF transcriptional co-activators. Mastering the molecular mechanisms regulating cardiomyocyte proliferation would permit the development of innovative strategies to stimulate cardiac regeneration in adult individuals, a hitherto unachieved yet fundamental therapeutic goal.

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This article was published in the following journal.

Name: The FEBS journal
ISSN: 1742-4658
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