Clock Dysfunction Triggers Fibrotic Response in the Heart

What is the role of the circadian clock component Bmal1 in cardiac function? Deputy Editor Merry Lindsey (University of Mississippi Medical Center) interviews lead author Ganesh Halade (University of Alabama at Birmingham) and expert Amanda Le Blanc (University of Louisville) in this engaging podcast about the work by the Young and Halade laboratories, which found a “striking” result: cardiomyocyte specific Bmal1 deletion not only triggered the development of diastolic dysfunction, adverse extracellular matrix remodeling, and inflammation, but also drastically reduced the lifespan of mice compared to control litter mates. Do the Ingle et al results indicate that cardiomyocytes are an early, upstream regulator of aging in the heart? Listen and learn.


Kevin A. Ingle, Vasundhara Kain, Mehak Goel, Sumanth D. Prabhu, Martin E. Young, Ganesh V Halade Cardiomyocyte specific Bmal1 deletion in mice triggers diastolic dysfunction, extracellular matrix response and impaired resolution of inflammation Am J Physiol Heart Circ Physiol, published online October 2, 2015, DOI: 10.1152/ajpheart.00608.2015.

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