ArticleCell death & disease2011
Metabolic stress promotes renal tubular inflammation by triggering the unfolded protein response.
Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 48 citations in OpenAlex.
- Effects of Individual Essential Amino Acids on Growth Rates of Young Rats Fed a Low-Protein Diet.Animals : an open access journal from MDPI · 2024Article
- Renoprotective effect ofIranian journal of basic medical sciences · 2024Article
- Comprehensive molecular and cellular characterization of endoplasmic reticulum stress-related key genes in renal ischemia/reperfusion injury.Frontiers in immunology · 2024Article
- Review
- BM-MSCs alleviate diabetic nephropathy in male rats by regulating ER stress, oxidative stress, inflammation, and apoptotic pathways.Frontiers in pharmacology · 2023Article
- Naringenin Alleviates Renal Ischemia Reperfusion Injury by Suppressing ER Stress-Induced Pyroptosis and Apoptosis through Activating Nrf2/HO-1 Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Ischemia-Like Stress Conditions Stimulate Trophic Activities of Adipose-Derived Stromal/Stem Cells.Cells · 2020Article
- Inhibition of oxygen-sensing prolyl hydroxylases increases lipid accumulation in human primary tubular epithelial cells without inducing ER stress.Cell and tissue research · 2020Article
- CD154 Induces Interleukin-6 Secretion by Kidney Tubular Epithelial Cells under Hypoxic Conditions: Inhibition by Chloroquine.Mediators of inflammation · 2020Article
- Arthropods Under Pressure: Stress Responses and Immunity at the Pathogen-Vector Interface.Frontiers in immunology · 2020Review
- Contribution of the Unfolded Protein Response (UPR) to the Pathogenesis of Proteasome-Associated Autoinflammatory Syndromes (PRAAS).Frontiers in immunology · 2019Review
- Reduced intestinal epithelial mitochondrial function enhances in vitro interleukin-8 production in response to commensal Escherichia coli.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Endoplasmic reticulum stress in the pathogenesis of fibrotic disease.The Journal of clinical investigation · 2018Review
- D-serine, a novel uremic toxin, induces senescence in human renal tubular cells via GCN2 activation.Scientific reports · 2017Article
- Impact of high cholesterol and endoplasmic reticulum stress on metabolic diseases: An updated mini-review.Redox biology · 2017Review
- Inflammation, oxidative stress, apoptosis, and autophagy in diabetes mellitus and diabetic kidney disease: the Four Horsemen of the Apocalypse.International urology and nephrology · 2017Review
- An endoplasmic reticulum stress-regulated lncRNA hosting a microRNA megacluster induces early features of diabetic nephropathy.Nature communications · 2016Article
- Ischaemic and inflammatory injury in renal graft from brain death donation: an update review.Journal of anesthesia · 2016Review
- Dengue-induced autophagy, virus replication and protection from cell death require ER stress (PERK) pathway activation.Cell death & disease · 2016Article
- Endoplasmic Reticulum Stress in the Diabetic Kidney, the Good, the Bad and the Ugly.Journal of clinical medicine · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The renal epithelium contributes to the development of inflammation during ischemic injury. Ischemia induces endoplasmic reticulum (ER) stress and activates the unfolded protein response (UPR). Ischemic tissues generate distress signals and inflammation that activates fibrogenesis and may promote adaptive immunity. Interestingly, the UPR may activate inflammation pathways. Our aim was to test whether the UPR is activated during metabolic stress and mediates a tubular inflammatory response. Glucose deprivation, not hypoxia and amino acids deprivation, activated the UPR in human renal cortical tubular cells in culture. This stress activated NF-κB and promoted the transcription of proinflammatory cytokines and chemokines, including IL-6, IL-8, TNF-α, RANTES and MCP-1. The protein kinase RNA (PKR)-like ER kinase signaling pathway was not required for the induction of inflammation but amplified cytokine. Inositol-requiring enzyme 1 activated NF-κB signaling and was required for the transcription of proinflammatory cytokines and chemokines following metabolic stress. Moreover, acute ischemia activated ER stress and inflammation in rat kidneys. Finally, the ER stress marker GRP78 and NF-κB p65/RelA were coexpressed in human kidney transplants biopsies performed before implantation, suggesting that ER stress activates tubular inflammation in human renal allografts. In conclusion, this study establishes a link between ischemic stress, the activation of the UPR and the generation of a tubular inflammatory response.
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