The functions of IRE1α in neurodegenerative diseases: Beyond ER stress

Chen, Ling; Bi, Minghong; Zhang, Zhen; Du, Xixun; Chen, Xi; Jiao, Qian; Jiang, Hong

doi:10.1016/j.arr.2022.101774

Cited by 2 publications

(2 citation statements)

References 194 publications

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“… 19 , 20 The ribonucleas(RNase) structural domain can cleave X-box binding protein 1 (XBP1) to convert it into a spliced form, the active transcription factor spliced XBP1. 21 , 22 XBP1 messenger RNA(mRNA) is the only characterized target of mammalian IRE1α ribonucleas activity. 23 Presentation of cleaved XBP1 to the nucleus elicits UPR-related target genes such as GRP78, glucose-regulated protein 94, and XBP1.…”

Section: Regulation Of Ers and Uprmentioning

confidence: 99%

Endoplasmic reticulum stress-mediated cell death in cardiovascular disease

An,

Wang,

Guan

et al. 2024

Cell Stress and Chaperones

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Section: Regulation Of Ers and Uprmentioning

confidence: 99%

Endoplasmic reticulum stress-mediated cell death in cardiovascular disease

An,

Wang,

Guan

et al. 2024

Cell Stress and Chaperones

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“…This pathway may induce p53 activation and lead to the upregulation of Bcl-2 associated X (BAX) protein, which triggers the release of cytochrome C (Cyt C) from the mitochondria to the cytosol and cause apoptotic neuronal cell death (Stefani et al, 2012 ). Furthermore, the RNase activity of IRE1α plays a critical role in splicing the mRNA coding for X-box binding protein 1 (XBP1) and increases the expression of genes involved in ER machinery, such as BiP (Lee et al, 2003 ; Hirota et al, 2006 ; Chen et al, 2022 ). Besides outlined functions, IRE1α participates in the degradation of some mRNAs and microRNAs, known as “regulated IRE1α-dependent decay” (RIDD; Hetz and Saxena, 2017 ; Figure 1B ).…”

Section: Er Stress-induced Cell Death In Neurodegenerative Diseasesmentioning

confidence: 99%

The neuroprotective effects of targeting key factors of neuronal cell death in neurodegenerative diseases: The role of ER stress, oxidative stress, and neuroinflammation

Karvandi

Hesari

Aref

et al. 2023

Front. Cell. Neurosci.

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Neuronal loss is one of the striking causes of various central nervous system (CNS) disorders, including major neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and Amyotrophic lateral sclerosis (ALS). Although these diseases have different features and clinical manifestations, they share some common mechanisms of disease pathology. Progressive regional loss of neurons in patients is responsible for motor, memory, and cognitive dysfunctions, leading to disabilities and death. Neuronal cell death in neurodegenerative diseases is linked to various pathways and conditions. Protein misfolding and aggregation, mitochondrial dysfunction, generation of reactive oxygen species (ROS), and activation of the innate immune response are the most critical hallmarks of most common neurodegenerative diseases. Thus, endoplasmic reticulum (ER) stress, oxidative stress, and neuroinflammation are the major pathological factors of neuronal cell death. Even though the exact mechanisms are not fully discovered, the notable role of mentioned factors in neuronal loss is well known. On this basis, researchers have been prompted to investigate the neuroprotective effects of targeting underlying pathways to determine a promising therapeutic approach to disease treatment. This review provides an overview of the role of ER stress, oxidative stress, and neuroinflammation in neuronal cell death, mainly discussing the neuroprotective effects of targeting pathways or molecules involved in these pathological factors.

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The functions of IRE1α in neurodegenerative diseases: Beyond ER stress

Cited by 2 publications

References 194 publications

Endoplasmic reticulum stress-mediated cell death in cardiovascular disease

Endoplasmic reticulum stress-mediated cell death in cardiovascular disease

The neuroprotective effects of targeting key factors of neuronal cell death in neurodegenerative diseases: The role of ER stress, oxidative stress, and neuroinflammation

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