The ubiquitin-proteasome system: A potential therapeutic target for heart failure

Standard

The ubiquitin-proteasome system: A potential therapeutic target for heart failure. / Barac, Yaron D; Emrich, Fabian; Krutzwakd-Josefson, Efrat; Schrepfer, Sonja; Sampaio, Luiz C; Willerson, James T; Robbins, Robert C; Ciechanover, Aaron; Mohr, Friedrich-Wilhelm; Aravot, Dan; Taylor, Doris A.

in: J HEART LUNG TRANSPL, Jahrgang 36, Nr. 7, 07.2017, S. 708-714.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ReviewForschung

Harvard

Barac, YD, Emrich, F, Krutzwakd-Josefson, E, Schrepfer, S, Sampaio, LC, Willerson, JT, Robbins, RC, Ciechanover, A, Mohr, F-W, Aravot, D & Taylor, DA 2017, 'The ubiquitin-proteasome system: A potential therapeutic target for heart failure', J HEART LUNG TRANSPL, Jg. 36, Nr. 7, S. 708-714. https://doi.org/10.1016/j.healun.2017.02.012

APA

Barac, Y. D., Emrich, F., Krutzwakd-Josefson, E., Schrepfer, S., Sampaio, L. C., Willerson, J. T., Robbins, R. C., Ciechanover, A., Mohr, F-W., Aravot, D., & Taylor, D. A. (2017). The ubiquitin-proteasome system: A potential therapeutic target for heart failure. J HEART LUNG TRANSPL, 36(7), 708-714. https://doi.org/10.1016/j.healun.2017.02.012

Vancouver

Bibtex

@article{c1bff071d2cd486f997fcf13f2871d7e,
title = "The ubiquitin-proteasome system: A potential therapeutic target for heart failure",
abstract = "The rising incidence of heart failure (HF) is one of the biggest challenges in cardiovascular medicine. The persistent shortage of donor organs for transplantation has led to an expanding application of left ventricular assist devices as a bridge to recovery. Accumulating evidence suggests that the ubiquitin-proteasome system (UPS), which is responsible for protein degradation, plays a direct role in cardiac hypertrophy and HF and is impacted by mechanical unloading. The UPS system also plays a role in the cardiac regulation of apoptosis, cell mass, and sarcomere quality control. Furthermore, it is a key regulator of β2-adrenergic signaling, cell excitability, and conductance. In this review, we discuss the roles of the UPS in cardiac health and disease, including its roles in the pathologic hypertrophy associated with HF and its reversal during mechanical unloading. Finally, we suggest future areas of research, including possible therapeutic strategies for reversing cardiac remodeling by targeting the UPS.",
keywords = "Heart Failure/etiology, Humans, Proteasome Endopeptidase Complex/physiology, Signal Transduction, Ubiquitin/physiology, Ventricular Remodeling",
author = "Barac, {Yaron D} and Fabian Emrich and Efrat Krutzwakd-Josefson and Sonja Schrepfer and Sampaio, {Luiz C} and Willerson, {James T} and Robbins, {Robert C} and Aaron Ciechanover and Friedrich-Wilhelm Mohr and Dan Aravot and Taylor, {Doris A}",
note = "Copyright {\textcopyright} 2017 International Society for the Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.",
year = "2017",
month = jul,
doi = "10.1016/j.healun.2017.02.012",
language = "English",
volume = "36",
pages = "708--714",
journal = "J HEART LUNG TRANSPL",
issn = "1053-2498",
publisher = "Elsevier USA",
number = "7",

}

RIS

TY - JOUR

T1 - The ubiquitin-proteasome system: A potential therapeutic target for heart failure

AU - Barac, Yaron D

AU - Emrich, Fabian

AU - Krutzwakd-Josefson, Efrat

AU - Schrepfer, Sonja

AU - Sampaio, Luiz C

AU - Willerson, James T

AU - Robbins, Robert C

AU - Ciechanover, Aaron

AU - Mohr, Friedrich-Wilhelm

AU - Aravot, Dan

AU - Taylor, Doris A

N1 - Copyright © 2017 International Society for the Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.

PY - 2017/7

Y1 - 2017/7

N2 - The rising incidence of heart failure (HF) is one of the biggest challenges in cardiovascular medicine. The persistent shortage of donor organs for transplantation has led to an expanding application of left ventricular assist devices as a bridge to recovery. Accumulating evidence suggests that the ubiquitin-proteasome system (UPS), which is responsible for protein degradation, plays a direct role in cardiac hypertrophy and HF and is impacted by mechanical unloading. The UPS system also plays a role in the cardiac regulation of apoptosis, cell mass, and sarcomere quality control. Furthermore, it is a key regulator of β2-adrenergic signaling, cell excitability, and conductance. In this review, we discuss the roles of the UPS in cardiac health and disease, including its roles in the pathologic hypertrophy associated with HF and its reversal during mechanical unloading. Finally, we suggest future areas of research, including possible therapeutic strategies for reversing cardiac remodeling by targeting the UPS.

AB - The rising incidence of heart failure (HF) is one of the biggest challenges in cardiovascular medicine. The persistent shortage of donor organs for transplantation has led to an expanding application of left ventricular assist devices as a bridge to recovery. Accumulating evidence suggests that the ubiquitin-proteasome system (UPS), which is responsible for protein degradation, plays a direct role in cardiac hypertrophy and HF and is impacted by mechanical unloading. The UPS system also plays a role in the cardiac regulation of apoptosis, cell mass, and sarcomere quality control. Furthermore, it is a key regulator of β2-adrenergic signaling, cell excitability, and conductance. In this review, we discuss the roles of the UPS in cardiac health and disease, including its roles in the pathologic hypertrophy associated with HF and its reversal during mechanical unloading. Finally, we suggest future areas of research, including possible therapeutic strategies for reversing cardiac remodeling by targeting the UPS.

KW - Heart Failure/etiology

KW - Humans

KW - Proteasome Endopeptidase Complex/physiology

KW - Signal Transduction

KW - Ubiquitin/physiology

KW - Ventricular Remodeling

U2 - 10.1016/j.healun.2017.02.012

DO - 10.1016/j.healun.2017.02.012

M3 - SCORING: Review article

C2 - 28341100

VL - 36

SP - 708

EP - 714

JO - J HEART LUNG TRANSPL

JF - J HEART LUNG TRANSPL

SN - 1053-2498

IS - 7

ER -