Abstract
The integrity of the proteome in cardiac myocytes is critical for robust heart function. Proteome integrity in all cells is managed by protein homeostasis or proteostasis, which encompasses processes that maintain the balance of protein synthesis, folding, and degradation in ways that allow cells to adapt to conditions that present a potential challenge to viability (1). While there are processes in various cellular locations in cardiac myocytes that contribute to proteostasis, those in the cytosol, mitochondria and endoplasmic reticulum (ER) have dominant roles in maintaining cardiac contractile function. Cytosolic proteostasis has been reviewed elsewhere (2, 3); accordingly, this review focuses on proteostasis in the ER and mitochondria, and how they might influence each other and, thus, impact heart function in the settings of cardiac physiology and disease.
Highlights
Cytosolic proteostasis has been reviewed elsewhere [2, 3]; this review focuses on proteostasis in the endoplasmic reticulum (ER) and mitochondria, and how they might influence each other and, impact heart function in the settings of cardiac physiology and disease
While this study indicates that IRE1 and perhaps the transcription factor, XBP1, protect against the development of heart failure with preserved ejection fraction (HFpEF), the genes that are responsible for this protection have not been identified
The processes that govern mitochondrial and ER proteostasis are of critical importance for the adaptation of eukaryotic cells to environmental changes that risk proteome integrity
Summary
Edited by: Junichi Sadoshima, University of Medicine and Dentistry of New Jersey, United States. Specialty section: This article was submitted to Cardiovascular Metabolism, a section of the journal Frontiers in Cardiovascular Medicine. The integrity of the proteome in cardiac myocytes is critical for robust heart function. While there are processes in various cellular locations in cardiac myocytes that contribute to proteostasis, those in the cytosol, mitochondria and endoplasmic reticulum (ER) have dominant roles in maintaining cardiac contractile function. Cytosolic proteostasis has been reviewed elsewhere [2, 3]; this review focuses on proteostasis in the ER and mitochondria, and how they might influence each other and, impact heart function in the settings of cardiac physiology and disease
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