ReviewFrontiers in cell and developmental biology2019
Endoplasmic Reticulum Stress Coping Mechanisms and Lifespan Regulation in Health and Diseases.
Review in Frontiers in cell and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
53 citing papers in PubMed, 97 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- The role of mitochondrial fusion protein 2 in regulating ER stress in premature placental aging: A case-control study.Medicine · 2026Article
- The role of sleep disorders in orchestrating proteomic dysfunction and multi-morbidity.Molecular psychiatry · 2026Review
- 4-Phenylbutyrate mitigates renal pathology linked to ER stress related pathways in C57BL/6J mice with hindlimb unloading.Scientific reports · 2026Article
- RIP3 and MLKL regulate ER stress in alcohol-associated liver disease and pharmacological ER stress models: Insights beyond necroptosis.JHEP reports : innovation in hepatology · 2026Article
- RIP3 and MLKL regulate Hepatic ER stress in alcohol-associated liver disease and pharmacological ER stress models: insights beyond necroptosis.bioRxiv : the preprint server for biology · 2025Article
- Protective functions of liver X receptor α on calcified aortic valve: involvement of regulating endoplasmic reticulum-mediated osteogenic differentiation.Cardiovascular research · 2025Article
- Endoplasmic Reticulum Stress in Tuberculosis: Molecular Bases and Pathophysiological Implications in the Immunopathogenesis of the Disease.International journal of molecular sciences · 2025Review
- TUDCA modulates drug bioavailability to regulate resistance to acute ER stress inMolecular biology of the cell · 2025Article
- Lipid Oxidation at the Crossroads: Oxidative Stress and Neurodegeneration Explored inAntioxidants (Basel, Switzerland) · 2025Review
- Stress Induced Mitochondrial Hyperfusion (SIMH): A Concise Review on SIMH in Neurodegenerative Disorders and Other Diseases.Organelle (Tucson, Ariz.) · 2025Article
- Integrating Physical and Biochemical Cues for Muscle Engineering: Scaffolds and Graft Durability.Bioengineering (Basel, Switzerland) · 2024Review
- Mitochondria-Associated Membranes in Aging and Senescence.Aging and disease · 2024Review
- Replicative aging in yeast involves dynamic intron retention patterns associated with mRNA processing/export and protein ubiquitination.Microbial cell (Graz, Austria) · 2024Article
- Chronic stress-induced anxiety-like behavior, hippocampal oxidative, and endoplasmic reticulum stress are reversed by young plasma transfusion in aged adult rats.Iranian journal of basic medical sciences · 2024Article
- Bioinformatics Analysis and Experimental Validation of Endoplasmic Reticulum Stress-Related Genes in Osteoporosis.International journal of general medicine · 2024Article
- Soluble epoxide hydrolase-targeting PROTAC activates AMPK and inhibits endoplasmic reticulum stress.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Impaired intracellular CaScience signaling · 2023Article
- Insights into the underlying pathogenesis and therapeutic potential of endoplasmic reticulum stress in degenerative musculoskeletal diseases.Military Medical Research · 2023Review
- Impairment of RPN4, a transcription factor, induces ER stress and lipid abnormality in Saccharomyces cerevisiae.Molecular and cellular biochemistry · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple factors lead to proteostatic perturbations, often resulting in the aberrant accumulation of toxic misfolded proteins. Cells, from yeast to humans, can respond to sudden accumulation of secretory proteins within the endoplasmic reticulum (ER) through pathways such as the Unfolded Protein Response (UPR). The ability of cells to adapt the ER folding environment to the misfolded protein burden ultimately dictates cell fate. The aging process is a particularly important modifier of the proteostasis network; as cells age, both their ability to maintain this balance in protein folding/degradation and their ability to respond to insults in these pathways can break down, a common element of age-related diseases (including neurodegenerative diseases). ER stress coping mechanisms are central to lifespan regulation under both normal and disease states. In this review, we give a brief overview of the role of ER stress response pathways in age-dependent neurodegeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.