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急性肾损伤：探索内质网应激介导的细胞死亡

Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death.

作者信息

Cheng Cong, Yuan Yuan, Yuan Fang, Li Xin

机构信息

Xiangya Hospital, Central South University, Changsha, Hunan, China.

Department of Emergency, Changsha Hospital of Traditional Chinese Medicine (Changsha Eighth Hospital), Changsha, Hunan, China.

出版信息

Front Pharmacol. 2024 Feb 12;15:1308733. doi: 10.3389/fphar.2024.1308733. eCollection 2024.

DOI:10.3389/fphar.2024.1308733
PMID:38434710
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10905268/
Abstract

Acute kidney injury (AKI) is a global health problem, given its substantial morbidity and mortality rates. A better understanding of the mechanisms and factors contributing to AKI has the potential to guide interventions aimed at mitigating the risk of AKI and its subsequent unfavorable outcomes. Endoplasmic reticulum stress (ERS) is an intrinsic protective mechanism against external stressors. ERS occurs when the endoplasmic reticulum (ER) cannot deal with accumulated misfolded proteins completely. Excess ERS can eventually cause pathological reactions, triggering various programmed cell death (autophagy, ferroptosis, apoptosis, pyroptosis). This article provides an overview of the latest research progress in deciphering the interaction between ERS and different programmed cell death. Additionally, the report consolidates insights into the roles of ERS in AKI and highlights the potential avenues for targeting ERS as a treatment direction toward for AKI.

摘要

急性肾损伤（AKI）是一个全球性的健康问题，因其具有相当高的发病率和死亡率。更好地了解导致AKI的机制和因素，有可能指导旨在降低AKI风险及其后续不良后果的干预措施。内质网应激（ERS）是一种针对外部应激源的内在保护机制。当内质网（ER）无法完全处理积累的错误折叠蛋白时，就会发生ERS。过度的ERS最终会导致病理反应，引发各种程序性细胞死亡（自噬、铁死亡、凋亡、焦亡）。本文概述了在解读ERS与不同程序性细胞死亡之间相互作用方面的最新研究进展。此外，该报告整合了对ERS在AKI中的作用的见解，并强调了将ERS作为AKI治疗方向的潜在途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/04d3c8e1f43c/fphar-15-1308733-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/b68625581798/fphar-15-1308733-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/0440cba336d1/fphar-15-1308733-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/ddc7aa50f158/fphar-15-1308733-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/8fc21ca846e1/fphar-15-1308733-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/9f628374dab7/fphar-15-1308733-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/04d3c8e1f43c/fphar-15-1308733-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/b68625581798/fphar-15-1308733-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/0440cba336d1/fphar-15-1308733-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/ddc7aa50f158/fphar-15-1308733-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/8fc21ca846e1/fphar-15-1308733-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/9f628374dab7/fphar-15-1308733-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8508/10905268/04d3c8e1f43c/fphar-15-1308733-g006.jpg

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