The 26S proteasome is a multicatalytic threonine protease complex responsible for degradation of the majority of proteins in eukaryotic cells. In the last two decades, the ubiquitin proteasome system (UPS) has been increasingly recognized as an integral component in numerous biologic processes including cell proliferation, adaptation to stress, and cell death. The turnover of intracellular proteins inevitably affects the contributions of these molecules to cellular networks and pathways in any given tissue or organ, including the myocardium. Perturbations in the protein-degradation process have been shown to affect protein turnover and thereby affect the cardiac cell functions that these molecules are designated to carry out, engendering diseased cardiac phenotypes. Recent studies have implicated the role of proteasomes in stressed cardiac phenotypes including postischemia-reperfusion injury and cardiac remodeling (e.g., heart failure). The 26S proteasomes also appear to be susceptible to modulation by stresses (e.g., reactive oxygen species). This review focuses on roles of the 26S proteasome system in protein degradation; it provides an overview of the progress made in cardiac proteasome research as well as a discussion of recent controversies regarding the UPS system in diseased cardiac phenotypes.

译文

26s蛋白酶体是一种多催化苏氨酸蛋白酶复合物,负责真核细胞中大多数蛋白质的降解。在过去的二十年中,泛素蛋白酶体系统 (UPS) 已被越来越多地视为许多生物学过程 (包括细胞增殖,对压力的适应和细胞死亡) 中不可或缺的组成部分。细胞内蛋白质的转换不可避免地影响这些分子对任何给定组织或器官 (包括心肌) 中细胞网络和途径的贡献。已显示蛋白质降解过程中的扰动会影响蛋白质的更新,从而影响这些分子被指定执行的心脏细胞功能,从而导致患病的心脏表型。最近的研究表明蛋白酶体在压力心脏表型中的作用,包括缺血后再灌注损伤和心脏重塑 (例如心力衰竭)。26s蛋白酶体似乎也容易受到压力 (例如活性氧) 的调节。这篇综述着重于26s蛋白酶体系统在蛋白质降解中的作用; 它概述了心脏蛋白酶体研究的进展,并讨论了有关UPS系统在患病心脏表型中的最新争议。

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