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Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation

Published Online: 2020-11-13

Published Print: 2021-02

Authors

Brown, Sean M.

Larsen, Nicholas K.

Thankam, Finosh G.

Agrawal, Devendra K https://orcid.org/0000-0001-5445-0013
Funding

Funding for this research was provided by:

National Institutes of Health (R01 HL128063)

National Institutes of Health (R01 HL144125)

National Institutes of Health (R01 HL147662)
License Information

Text and Data Mining valid from 2020-11-13

Version of Record valid from 2020-11-13
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Article History

Received: 29 July 2020

Accepted: 6 November 2020

First Online: 13 November 2020

Compliance with ethical standards

:

: The authors declare that they have no conflict of interest.

: In this critical review, we discussed critical molecular and cellular events, including fetal metabolic phenotype of glycolytic metabolism over fatty acid metabolism, involvement of ketone body metabolism, mitochondrial dysfunction, and the cellular effect of reactive oxygen species (ROS) in the underlying biochemical events associated with the molecular pathology of atrial fibrillation, especially with respect to structural, contractile, and electrophysiological properties. In addition, the article critically reviews the current understanding, potential demerits, and translational strategies in the management of AF.

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