ArticleFrontiers in physiology2012
The endoplasmic reticulum stress response in aging and age-related diseases.
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers.
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Who cites it
193 citing papers in PubMed, 381 citations in OpenAlex.
- Monocyte transcriptomic profile following EPA and DHA supplementation in men and women with low-grade chronic inflammation.Atherosclerosis · 2024Trial
- Fish oil supplementation induces expression of genes related to cell cycle, endoplasmic reticulum stress and apoptosis in peripheral blood mononuclear cells: a transcriptomic approach.Journal of internal medicine · 2014Trial
- 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
- Metabolite import by SLC33A1 is required for ATF6 activation during endoplasmic reticulum stress.Life science alliance · 2026Article
- Gene Expression Analysis of Mitochondria-Associated Membrane (MAM)-Related Genes in ER Stress and Alzheimer's Disease.Cellular and molecular neurobiology · 2026Article
- Age-dependent induction of ER stress in retinal pigment epithelium impairs phagocytosis via ADAM17-dependent MERTK shedding.The Journal of biological chemistry · 2026Article
- Intercompartmental communication in senescence.FEBS open bio · 2026Review
- Alcohol Consumption During Muscle Disuse Causes Differential Signaling Responses in a Muscle-Specific Manner in Mice.International journal of molecular sciences · 2026Article
- Reduction of calreticulin and ERp57 with age reveals the ER stress-related roles in cell viability and organismal lifespan regulation.Frontiers in aging · 2026Article
- The skeletal transcriptional response to mechanical load varies with age and tissue compartment in female mice.JBMR plus · 2025Article
- The science of bioelectrical impedance-derived phase angle: insights from body composition in youth.Reviews in endocrine & metabolic disorders · 2025Review
- Review
- The cell origin of reactive oxygen species and its implication for evolutionary trade-offs.Open biology · 2025Review
- Skeletal muscle atrophy induced by aging and disuse atrophy are strongly associated with the upregulation of the endoplasmic stress protein CHOP in rats.Molecular biology reports · 2025Article
- Article
- Aging triggers mitochondrial, endoplasmic reticulum, and metabolic stress responses in the heart.The journal of cardiovascular aging · 2025Article
- Anti-aging properties of the aminosterols of the dogfish shark.npj aging · 2024Review
- The role of T cells in vascular aging, hypertension, and atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2024Review
- Diet-induced obesity and aging-induced upregulation of Trib3 interfere with energy homeostasis by downregulating the thermogenic capacity of BAT.Experimental & molecular medicine · 2024Article
133 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The endoplasmic reticulum(ER) is a multifunctional organelle within which protein folding, lipid biosynthesis, and calcium storage occurs. Perturbations such as energy or nutrient depletion, disturbances in calcium or redox status that disrupt ER homeostasis lead to the misfolding of proteins, ER stress and up-regulation of several signaling pathways coordinately called the unfolded protein response (UPR). The UPR is characterized by the induction of chaperones, degradation of misfolded proteins and attenuation of protein translation. The UPR plays a fundamental role in the maintenance of cellular homeostasis and thus is central to normal physiology. However, sustained unresolved ER stress leads to apoptosis. Aging linked declines in expression and activity of key ER molecular chaperones and folding enzymes compromise proper protein folding and the adaptive response of the UPR. One mechanism to explain age associated declines in cellular functions and age-related diseases is a progressive failure of chaperoning systems. In many of these diseases, proteins or fragments of proteins convert from their normally soluble forms to insoluble fibrils or plaques that accumulate in a variety of organs including the liver, brain or spleen. This group of diseases, which typically occur late in life includes Alzheimer's, Parkinson's, type II diabetes and a host of less well known but often equally serious conditions such as fatal familial insomnia. The UPR is implicated in many of these neurodegenerative and familial protein folding diseases as well as several cancers and a host of inflammatory diseases including diabetes, atherosclerosis, inflammatory bowel disease and arthritis. This review will discuss age-related changes in the ER stress response and the role of the UPR in age-related diseases.
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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.