ArticleAmerican journal of physiology. Renal physiology2015
mTOR contributes to ER stress and associated apoptosis in renal tubular cells.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 68 citations in OpenAlex.
- Endoplasmic reticulum stress induced autophagy alters cellular processing of cationic lipid delivered siRNAs.Drug delivery and translational research · 2026Article
- Protein kinase R-like ER kinase (PERK) is involved in the endoplasmic reticulum stress response of its psyllid vector toMicrobiology spectrum · 2026Article
- Molecular mechanisms attributed to colistin renal proximal tubular epithelial cytotoxicity.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Review
- Endoplasmic reticulum-mediated organelle crosstalk in kidney disease.Nature reviews. Nephrology · 2025Review
- The role of the SIRT1 and mTOR pathways in exercise-induced β-cell senescence reduction in type 2 diabetes mellitus.Cellular and molecular life sciences : CMLS · 2025Review
- The Hidden Price of Plenty: Oxidative Stress and Calorie-Induced Cardiometabolic Dysfunction.Life (Basel, Switzerland) · 2025Review
- Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.BMC nephrology · 2025Review
- Peripheral Transcriptomics in Acute and Long-Term Kidney Dysfunction in SARS-CoV-2 Infection.Kidney360 · 2025Article
- Identifying Multiomic Signatures of X-Linked Retinoschisis-Derived Retinal Organoids and Mice Harboring Patient-Specific Mutation Using Spatiotemporal Single-Cell Transcriptomics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sestrin2 Attenuates Myocardial Endoplasmic Reticulum Stress and Cardiac Dysfunction During Ischemia/Reperfusion Injury.Journal of the American Heart Association · 2024Article
- Cell-vision fusion: A Swin transformer-based approach for predicting kinase inhibitor mechanism of action from Cell Painting data.iScience · 2024Article
- Augmented ERO1α upon mTORC1 activation induces ferroptosis resistance and tumor progression via upregulation of SLC7A11.Journal of experimental & clinical cancer research : CR · 2024Article
- Resolvin D1 alleviates apoptosis triggered by endoplasmic reticulum stress in IPEC-J2 cells.BMC veterinary research · 2024Article
- XBP1-mediated transcriptional regulation of SLC5A1 in human epithelial cells in disease conditions.Cell & bioscience · 2024Article
- Contaminants from dredged sediments alter the transcriptome of Manila clam and induce shifts in microbiota composition.BMC biology · 2023Article
- Research progress on endoplasmic reticulum homeostasis in kidney diseases.Cell death & disease · 2023Review
- Interconnected Adaptive Responses: A Way Out for Cancer Cells to Avoid Cellular Demise.Cancers · 2022Review
- Lysosomal Stress Response (LSR): Physiological Importance and Pathological Relevance.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Review
- CO-Releasing Molecule-2 Prevents Acute Kidney Injury through Suppression of ROS-Fyn-ER Stress Signaling in Mouse Model.Oxidative medicine and cellular longevity · 2021Article
- Bacterial Manipulation of the Integrated Stress Response: A New Perspective on Infection.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
ER stress has been implicated in the pathogenesis of both acute and chronic kidney diseases. However, the molecular regulation of ER stress in kidney cells and tissues remains poorly understood. In this study, we examined tunicamycin-induced ER stress in renal proximal tubular cells (RPTC). Tunicamycin induced the phosphorylation and activation of PERK and eIF2α within 2 h in RPTC, which was followed by the induction of GRP78 and CHOP. Consistently, tunicamycin also induced apoptosis in RPTC. Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K. Inhibition of mTOR with rapamycin partially suppressed the phosphorylation of PERK and eIF2a and the induction of CHOP and GRP78 induction during tunicamycin treatment. Rapamycin also inhibited apoptosis during tunicamycin treatment and increased cell survival. Collectively, the results suggest that mTOR plays a regulatory role in ER stress, and inhibition of mTOR may have potential therapeutic effects in ER stress-related renal 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 Socratic graph.