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

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

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.

Keywords: acute kidney injury; apoptosis; autophagy; endoplasmic reticulum stress; ferroptosis; pyroptosis.

Publication types

  • Review

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The manuscript was supported by the Hunan Provincial Key Laboratory of Anti-Resistance Microbial Drugs (No: 2023TP1013), the Changsha Science and Technology Project (No: kq2208464), the Project of Changsha Municipal Health Commission (No: KJ-B2023064).