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Acute kidney injury: exploring endoplasmic reticulum stress-mediated cell death
Summary
This review examines how endoplasmic reticulum stress, a cellular response to accumulated misfolded proteins, can trigger various forms of cell death in acute kidney injury. While not directly about microplastics, these same stress pathways are activated when cells are exposed to nanoplastics, which have been shown to accumulate in kidney tissue. Understanding these mechanisms helps explain how microplastic exposure could contribute to kidney damage at the cellular level.
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.
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