Demirel-Yalciner Tugce, Sozen Erdi, Ozer Nesrin Kartal
Department of Biochemistry, Faculty of Medicine, Marmara University, Maltepe, Turkey.
Genetic and Metabolic Diseases Research and Investigation Center (GEMHAM), Marmara University, Maltepe, Turkey.
Front Aging. 2022 Jan 20;2:790702. doi: 10.3389/fragi.2021.790702. eCollection 2021.
Aging is a physiological process defined by decreased cellular and tissue functions. Reduced capacity of protein degradation is one of the important hallmarks of aging that may lead to misfolded protein accumulation and progressive loss of function in organ systems. Recognition of unfolded/misfolded protein aggregates endoplasmic reticulum (ER) stress sensors activates an adaptive mechanism, the unfolded protein response (UPR). The initial step of UPR is defined by chaperone enhancement, ribosomal translation suppression, and misfolded protein degradation, while prolonged ER stress triggers apoptosis. MicroRNAs (miRNAs) are non-coding RNAs affecting various signaling pathways through degradation or translational inhibition of targeted mRNAs. Therefore, UPR and miRNA impairment in aging and age-related diseases is implicated in various studies. This review will highlight the recent insights in ER stress-miRNAs alterations during aging and age-related diseases, including metabolic, cardiovascular, and neurodegenerative diseases and several cancers.
衰老 是一种由细胞和组织功能衰退所定义的生理过程。蛋白质降解能力的下降是衰老的重要标志之一，这可能导致错误折叠的蛋白质积累以及器官系统功能的逐渐丧失。未折叠/错误折叠的蛋白质聚集体被内质网（ER）应激传感器识别后会激活一种适应性机制——未折叠蛋白反应（UPR）。UPR的初始步骤表现为伴侣蛋白增强、核糖体翻译抑制以及错误折叠蛋白的降解，而长期的内质网应激会引发细胞凋亡。微小RNA（miRNA）是一类非编码RNA，通过降解或抑制靶向mRNA的翻译来影响各种信号通路。因此，衰老及衰老相关疾病中的UPR和miRNA损伤在各种研究中都有涉及。本综述将重点介绍衰老及衰老相关疾病（包括代谢性疾病、心血管疾病、神经退行性疾病和几种癌症）期间内质网应激与微小RNA改变的最新见解。
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