Endoplasmic Reticulum Stress Signaling and Neuronal Cell Death

Merighi, Adalberto; Lossi, Laura

doi:10.3390/ijms232315186

Cited by 33 publications

(13 citation statements)

References 255 publications

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“…7E, many calcium homeostasis related proteins were downregulated after a long time of etoposide treatment, which might suggest imbalance of Ca 2+ metabolism 66,67 and perturbations in ER homeostasis. 68,69 The downregulation of unfolded protein response (UPR) related proteins (ERO1A, VCP) 70 and BAP31 (refs. 71 and 72) (a broad-specificity MP chaperone and quality control factor which could support ER and mitochondrial homeostasis) also suggested ER stress and occurrence of apoptosis.…”

Section: Resultsmentioning

confidence: 99%

Metal organic layers enabled cell surface engineering coupling biomembrane fusion for dynamic membrane proteome profiling

Jiang,

Wang,

Qiao

et al. 2023

Chem. Sci.

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Section: Resultsmentioning

confidence: 99%

Metal organic layers enabled cell surface engineering coupling biomembrane fusion for dynamic membrane proteome profiling

Jiang,

Wang,

Qiao

et al. 2023

Chem. Sci.

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“…(2) Metabolically linked proinflammatory stress, such as endoplasmic reticulum (ER) stress, modulates lipid metabolism and mediates the release of cytokines (IL-1α, IL-6, and IL-8), which are known to participate in age-related chronic inflammation [ 68 ]. ER stress triggers an unfolded protein response (UPR) and transcriptionally regulates lipogenesis [ 85 ], thus playing an essential role in lipid metabolism [ 85 , 86 , 87 , 88 ]. (3) Stress damage such as DNA damage and response play a major role in cellular senescence in vitro [ 89 ].…”

Section: Discussionmentioning

confidence: 99%

Genetic Networks of Alzheimer’s Disease, Aging, and Longevity in Humans

Balmorez

Sakazaki

Murakami

2023

IJMS

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Human genomic analysis and genome-wide association studies (GWAS) have identified genes that are risk factors for early and late-onset Alzheimer’s disease (AD genes). Although the genetics of aging and longevity have been extensively studied, previous studies have focused on a specific set of genes that have been shown to contribute to or are a risk factor for AD. Thus, the connections among the genes involved in AD, aging, and longevity are not well understood. Here, we identified the genetic interaction networks (referred to as pathways) of aging and longevity within the context of AD by using a gene set enrichment analysis by Reactome that cross-references more than 100 bioinformatic databases to allow interpretation of the biological functions of gene sets through a wide variety of gene networks. We validated the pathways with a threshold of p-value < 1.00 × 10−5 using the databases to extract lists of 356 AD genes, 307 aging-related (AR) genes, and 357 longevity genes. There was a broad range of biological pathways involved in AR and longevity genes shared with AD genes. AR genes identified 261 pathways within the threshold of p < 1.00 × 10−5, of which 26 pathways (10% of AR gene pathways) were further identified by overlapping genes among AD and AR genes. The overlapped pathways included gene expression (p = 4.05 × 10−11) including ApoE, SOD2, TP53, and TGFB1 (p = 2.84 × 10−10); protein metabolism and SUMOylation, including E3 ligases and target proteins (p = 1.08 × 10−7); ERBB4 signal transduction (p = 2.69 × 10−6); the immune system, including IL-3 and IL-13 (p = 3.83 × 10−6); programmed cell death (p = 4.36 × 10−6); and platelet degranulation (p = 8.16 × 10−6), among others. Longevity genes identified 49 pathways within the threshold, of which 12 pathways (24% of longevity gene pathways) were further identified by overlapping genes among AD and longevity genes. They include the immune system, including IL-3 and IL-13 (p = 7.64 × 10−8), plasma lipoprotein assembly, remodeling and clearance (p < 4.02 × 10−6), and the metabolism of fat-soluble vitamins (p = 1.96 × 10−5). Thus, this study provides shared genetic hallmarks of aging, longevity, and AD backed up by statistical significance. We discuss the significant genes involved in these pathways, including TP53, FOXO, SUMOylation, IL4, IL6, APOE, and CEPT, and suggest that mapping the gene network pathways provide a useful basis for further medical research on AD and healthy aging.

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“…When the cell’s adaptive reaction to ER stress falls short, programmed cell death is initiated through multiple mechanisms. These mechanisms encompass the IRE1-activated ASK1/JNK signaling, the PERK/eIF2-supported activation of the proapoptotic transcription factor CHOP, Bax/Bak-mediated calcium release into the cytosol, and the proteolytic stimulation of procaspase-12 ( Merighi and Lossi, 2022 ). IRE1α stands out as one of the highly conserved sensors for ER stress.…”

Section: Endoplasmic Reticulum Stress and Apoptosismentioning

confidence: 99%

Orexins in apoptosis: a dual regulatory role

Cavalu,

Saber,

Hamad

et al. 2024

Front. Cell. Neurosci.

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The orexins, also referred to as hypocretins, are neuropeptides that originate from the lateral hypothalamus (LH) region of the brain. They are composed of two small peptides, orexin-A, and orexin-B, which are broadly distributed throughout the central and peripheral nervous systems. Orexins are recognized to regulate diverse functions, involving energy homeostasis, the sleep-wake cycle, stress responses, and reward-seeking behaviors. Additionally, it is suggested that orexin-A deficiency is linked to sleepiness and narcolepsy. The orexins bind to their respective receptors, the orexin receptor type 1 (OX1R) and type 2 (OX2R), and activate different signaling pathways, which results in the mediation of various physiological functions. Orexin receptors are widely expressed in different parts of the body, including the skin, muscles, lungs, and bone marrow. The expression levels of orexins and their receptors play a crucial role in apoptosis, which makes them a potential target for clinical treatment of various disorders. This article delves into the significance of orexins and orexin receptors in the process of apoptosis, highlighting their expression levels and their potential contributions to different diseases. The article offers an overview of the existing understanding of the orexin/receptor system and how it influences the regulation of apoptosis.

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Endoplasmic Reticulum Stress Signaling and Neuronal Cell Death

Cited by 33 publications

References 255 publications

Metal organic layers enabled cell surface engineering coupling biomembrane fusion for dynamic membrane proteome profiling

Metal organic layers enabled cell surface engineering coupling biomembrane fusion for dynamic membrane proteome profiling

Genetic Networks of Alzheimer’s Disease, Aging, and Longevity in Humans

Orexins in apoptosis: a dual regulatory role

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