Next Article in Journal
Resolved Hyperfine at L-band for High-Spin CoEDTA, A Model for Co Sites in Proteins
Previous Article in Journal
Quantification of 3D Brain Microangioarchitectures in an Animal Model of Krabbe Disease
Previous Article in Special Issue
Delayed Onset of Age-Dependent Changes in Ultrastructure of Myocardial Mitochondria as One of the Neotenic Features in Naked Mole Rats (Heterocephalus glaber)
Article Menu

Export Article

Open AccessReview

Altered Intracellular Calcium Homeostasis and Arrhythmogenesis in the Aged Heart

1
Dorothy M. Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
2
Department of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(10), 2386; https://doi.org/10.3390/ijms20102386
Received: 12 April 2019 / Revised: 29 April 2019 / Accepted: 8 May 2019 / Published: 14 May 2019
(This article belongs to the Special Issue The Impact of Aging on Cardio and Cerebrovascular Diseases)
  |  
PDF [688 KB, uploaded 14 May 2019]
  |  

Abstract

Aging of the heart is associated with a blunted response to sympathetic stimulation, reduced contractility, and increased propensity for arrhythmias, with the risk of sudden cardiac death significantly increased in the elderly population. The altered cardiac structural and functional phenotype, as well as age-associated prevalent comorbidities including hypertension and atherosclerosis, predispose the heart to atrial fibrillation, heart failure, and ventricular tachyarrhythmias. At the cellular level, perturbations in mitochondrial function, excitation-contraction coupling, and calcium homeostasis contribute to this electrical and contractile dysfunction. Major determinants of cardiac contractility are the intracellular release of Ca2+ from the sarcoplasmic reticulum by the ryanodine receptors (RyR2), and the following sequestration of Ca2+ by the sarco/endoplasmic Ca2+-ATPase (SERCa2a). Activity of RyR2 and SERCa2a in myocytes is not only dependent on expression levels and interacting accessory proteins, but on fine-tuned regulation via post-translational modifications. In this paper, we review how aberrant changes in intracellular Ca2+ cycling via these proteins contributes to arrhythmogenesis in the aged heart. View Full-Text
Keywords: calcium signaling; cardiac arrhythmia; ageing; ryanodine receptor; sarco/endoplasmic Ca2+-ATPase calcium signaling; cardiac arrhythmia; ageing; ryanodine receptor; sarco/endoplasmic Ca2+-ATPase
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Hamilton, S.; Terentyev, D. Altered Intracellular Calcium Homeostasis and Arrhythmogenesis in the Aged Heart. Int. J. Mol. Sci. 2019, 20, 2386.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top