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Journal of Cellular Signaling

ISSN: 2692-0638

Review Article Open Access
Volume 2 | Issue 3 | DOI: https://doi.org/10.33696/Signaling.2.048

NH2-Terminal Cleavage of Cardiac Troponin I Signals Adaptive Response to Cardiac Stressors

Chad M. Warren1,#, Monika Halas1,#, Han-Zhong Feng1, Beata M. Wolska1,2, Jian-Ping Jin1, R. John Solaro1,*
  • 1Department of Physiology & Biophysics, Center for Cardiovascular Research, University of Illinois at Chicago, USA
  • 2Division of Cardiology, Center for Cardiovascular Research, University of Illinois at Chicago, USA
  • #These authors made equal contributions to this manuscript
+ Affiliations - Affiliations

Corresponding Author

R. John Solaro, solarorj@uic.edu

Received Date: July 26, 2021

Accepted Date: August 16, 2021

Citation:

Warren CM, Halas M, Feng HZ, Wolska BM, Jin JP, Solaro RJ. NH2-Terminal Cleavage of Cardiac Troponin I Signals Adaptive Response to Cardiac Stressors. J Cell Signal. 2021;2(3):162-171.


Copyright: © 2021 Warren CM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Cardiac sarcomeres express a variant of troponin I (cTnI) that contains a unique N-terminal extension of ~30 amino acids with regulatory phosphorylation sites. The extension is important in the control of myofilament response to Ca2+, which contributes to the neuro-humoral regulation of the dynamics of cardiac contraction and relaxation. Hearts of various species including humans express a stress-induced truncated variant of cardiac troponin I (cTnI-ND) missing the first ~30 amino acids and functionally mimicking the phosphorylated state of cTnI. Studies have demonstrated that upregulation of cTnI-ND potentially represents a homeostatic mechanism as well as an adaptive response in pathophysiology including ischemia/reperfusion injury, beta adrenergic maladaptive activation, and aging. We present evidence showing that cTnI-ND can modify the trigger for hypertrophic cardiomyopathy (HCM) by reducing the Ca2+ sensitivity of myofilaments from hearts with an E180G mutation in α-tropomyosin. Induction of this truncation may represent a therapeutic approach to modifying Ca2+-responses in hearts with hypercontractility or heat failure with preserved ejection fraction.

Keywords

Sarcomeres, Ca2+-sensitivity, Hypertrophic cardiomyopathy, Heart failure, Tropomyosin

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