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    Cardiac cells generate and amplify force in the context of cardiac load, yet the membranous sheath enclosing the muscle fibers-the sarcolemma-does not experience displacement. That the sarcolemma sustains beat-to-beat pressure changes without experiencing significant distortion is a muscle-contraction paradox. Here, we report that an elastic element-the motor protein prestin (Slc26a5)-serves to amplify actin-myosin force generation in mouse and human cardiac myocytes, accounting partly for the nonlinear capacitance of cardiomyocytes. The functional significance of prestin is underpinned by significant alterations of cardiac contractility in Prestin-knockout mice. Prestin was previously considered exclusive to the inner ear's outer hair cells; however, our results show that prestin serves a broader cellular motor function. Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.


    Xiao-Dong Zhang, Phung N Thai, Lu Ren, Maria Cristina Perez Flores, Hannah A Ledford, Seojin Park, Jeong Han Lee, Choong-Ryoul Sihn, Che-Wei Chang, Wei Chun Chen, Valeriy Timofeyev, Jian Zuo, James W Chan, Ebenezer N Yamoah, Nipavan Chiamvimonvat. Prestin amplifies cardiac motor functions. Cell reports. 2021 May 04;35(5):109097

    PMID: 33951436

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