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STAT3: a link between CaMKII–βIV-spectrin and maladaptive remodeling?
Mohit Hulsurkar, … , Ann P. Quick, Xander H.T. Wehrens
Mohit Hulsurkar, … , Ann P. Quick, Xander H.T. Wehrens
Published November 12, 2018
Citation Information: J Clin Invest. 2018;128(12):5219-5221. https://doi.org/10.1172/JCI124778.
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Commentary Article has an altmetric score of 2

STAT3: a link between CaMKII–βIV-spectrin and maladaptive remodeling?

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Abstract

βIV-Spectrin, along with ankyrin and Ca2+/calmodulin-dependent kinase II (CaMKII), has been shown to form local signaling domains at the intercalated disc, while playing a key role in the regulation of Na+ and K+ channels in cardiomyocytes. In this issue of the JCI, Unudurthi et al. show that under chronic pressure overload conditions, CaMKII activation leads to βIV-spectrin degradation, resulting in the release of sequestered STAT3 from the intercalated discs. This in turn leads to dysregulation of STAT3-mediated gene transcription, maladaptive remodeling, fibrosis, and decreased cardiac function. Overall, this study presents interesting findings regarding the role of CaMKII and βIV-spectrin under physiological as well as pathological conditions.

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Mohit Hulsurkar, Ann P. Quick, Xander H.T. Wehrens

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