ArticleCell death & disease2024
DDRGK1-mediated ER-phagy attenuates acute kidney injury through ER-stress and apoptosis.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 25 citations in OpenAlex.
- Mitochondria-associated endoplasmic reticulum membranes and calcium ion exchange: A novel direction for aging and neurodegenerative diseases.Neural regeneration research · 2026Article
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Redox control at the ER-mitochondria interface in kidney transplantation: MAM-centered stress signaling and translational organoid platforms.Redox biology · 2026Review
- uPAR/suPAR Signaling and Organ Crosstalk in Cardiovascular-Kidney-Metabolic Syndrome.Circulation research · 2026Review
- Autophagy-epithelial-mesenchymal transition crosstalk in acute respiratory distress syndrome: Mechanistic insights and therapeutic perspectives (Review).Experimental and therapeutic medicine · 2026Review
- DDRGK1 regulates muscle development by maintaining mitochondrial calcium homeostasis and oxidative phosphorylation via stabilizing IP3R.Molecular biology reports · 2026Article
- ATF6 ameliorates renal warm ischemia-reperfusion injury through FHL2-mediated NF-κB signaling pathway.iScience · 2026Article
- UFMylation of Pyruvate Dehydrogenase Regulates Mitochondrial Metabolism.bioRxiv : the preprint server for biology · 2026Article
- XIAP Stabilizes DDRGK1 to Promote ER-Phagy and Protects Against Noise-Induced Hearing Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- The multiple roles of Ggt1-Cre in the generation of transgenic mice.Cellular & molecular biology letters · 2026Article
- Fecal microbiota transplantation ameliorates radiation-induced lung injury by reshaping gut metabolic homeostasis to activate FAM134B-mediated ER-phagy.PLoS pathogens · 2026Article
- From organelles to therapy: rethinking combined hepatocellular-cholangiocarcinoma.Frontiers in cell and developmental biology · 2026Review
- Diabetic kidney disease: exploring mechanistic depths and the future of pharmacological intervention.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The dysregulated unfolded protein response in diabetic kidney disease: mechanisms and crosstalk with cell death pathways.Frontiers in pharmacology · 2026Review
- Endoplasmic reticulum stress-mediated programmed cell death in the tumor microenvironment.Cell death discovery · 2025Review
- Article
- Improved bioavailability and anti-nephrotoxicity efficacy of polydatin on cisplatin-induced AKIInternational journal of pharmaceutics: X · 2025Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Placental RTN3L-dependent ER-Phagy Contributes to Fetal Testicular Dysplasia Upon Environmental Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Acute kidney injury (AKI) constitutes a prevalent clinical syndrome characterized by elevated morbidity and mortality rates, emerging as a significant public health issue. This study investigates the interplay between endoplasmic reticulum (ER) stress, unfolded protein response (UPR), and ER-associated degradation (ER-phagy) in the pathogenesis of AKI. We employed four distinct murine models of AKI-induced by contrast media, ischemia-reperfusion injury, cisplatin, and folic acid-to elucidate the relationship between ER-phagy, ER stress, and apoptosis. Our findings reveal a marked decrease in ER-phagy coinciding with an accumulation of damaged ER, elevated ER stress, and increased apoptosis across all AKI models. Importantly, overexpression of DDRGK1 in HK-2 cells enhanced ER-phagy levels, ameliorating contrast-induced ER stress and apoptosis. These findings unveil a novel protective mechanism in AKI, wherein DDRGK1-UFL1-mediated ER-phagy mitigates ER stress and apoptosis in renal tubular epithelial cells. Our results thereby contribute to understanding the molecular underpinnings of AKI and offer potential therapeutic targets for its treatment.
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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.