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Retraction Open Access | 10.1172/jci.insight.146654

Disruption of embryonic ROCK signaling reproduces the sarcomeric phenotype of hypertrophic cardiomyopathy

Kate E. Bailey, Guy A. MacGowan, Simon Tual-Chalot, Lauren Phillips, Timothy J. Mohun, Deborah J. Henderson, Helen M. Arthur, Simon D. Bamforth, and Helen M. Phillips

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Published December 17, 2020 - More info

Published in Volume 5, Issue 24 on December 17, 2020
JCI Insight. 2020;5(24):e146654. https://doi.org/10.1172/jci.insight.146654.
© 2020 cardiomyopathy et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published December 17, 2020 - Version history
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Related article:

Disruption of embryonic ROCK signaling reproduces the sarcomeric phenotype of hypertrophic cardiomyopathy
Kate E. Bailey, … , Simon D. Bamforth, Helen M. Phillips
Kate E. Bailey, … , Simon D. Bamforth, Helen M. Phillips
Disruption of ROCK activity in embryonic cardiomyocytes revealed a developmental origin for hypertrophic cardiomyopathy.
Research Article Cardiology

Disruption of embryonic ROCK signaling reproduces the sarcomeric phenotype of hypertrophic cardiomyopathy

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Abstract

Sarcomeric disarray is a hallmark of gene mutations in patients with hypertrophic cardiomyopathy (HCM). However, it is unknown when detrimental sarcomeric changes first occur and whether they originate in the developing embryonic heart. Furthermore, Rho kinase (ROCK) is a serine/threonine protein kinase that is critical for regulating the function of several sarcomeric proteins, and therefore, our aim was to determine whether disruption of ROCK signaling during the earliest stages of heart development would disrupt the integrity of sarcomeres, altering heart development and function. Using a mouse model in which the function of ROCK is specifically disrupted in embryonic cardiomyocytes, we demonstrate a progressive cardiomyopathy that first appeared as sarcomeric disarray during cardiogenesis. This led to abnormalities in the structure of the embryonic ventricular wall and compensatory cardiomyocyte hypertrophy during fetal development. This sarcomeric disruption and hypertrophy persisted throughout adult life, triggering left ventricular concentric hypertrophy with systolic dysfunction, and reactivation of fetal gene expression and cardiac fibrosis, all typical features of HCM. Taken together, our findings establish a mechanism for the developmental origin of the sarcomeric phenotype of HCM and suggest that variants in the ROCK genes or disruption of ROCK signaling could, in part, contribute to its pathogenesis.

Authors

Kate E. Bailey, Guy A. MacGowan, Simon Tual-Chalot, Lauren Phillips, Timothy J. Mohun, Deborah J. Henderson, Helen M. Arthur, Simon D. Bamforth, Helen M. Phillips

×

Original citation: JCI Insight. 2019;4(8):e125172. https://doi.org/10.1172/jci.insight.125172

Citation for this retraction: JCI Insight. 2020;5(24):e146654. https://doi.org/10.1172/jci.insight.146654

Newcastle University recently notified JCI Insight of data manipulation in this article. In accordance with the institutional recommendation and at the request of the corresponding author, JCI Insight is retracting this article.

Footnotes

See the related article at Disruption of embryonic ROCK signaling reproduces the sarcomeric phenotype of hypertrophic cardiomyopathy.

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  • Version 1 (December 17, 2020): Electronic publication

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