ArticleCell death discovery2023
Vitamin D receptor attenuate ischemia-reperfusion kidney injury via inhibiting ATF4.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- CLPP loss confers sex-specific protection from renal ischemia reperfusion injury.Redox biology · 2026Article
- Integrated Stress Response and Drug-Induced Acute Kidney Injury: Involvement of Activating ATF4-STAT1-GBP2 Signaling.Journal of the American Society of Nephrology : JASN · 2026Article
- mJournal of cardiothoracic surgery · 2026Article
- Vitamin D/VDR Signaling and Programmed Cell Death in Sepsis-Associated Organ Injury: Evidence from Sepsis and Related Disease Models.Journal of inflammation research · 2026Review
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- ATF3 aggravates kidney fibrosis via HDAC6-dependent epigenetic reprogramming.International journal of biological sciences · 2026Article
- Vitamin D receptor modulates autophagy via miR-20a-5p/ATG16L1 axis to alleviate lipopolysaccharide-induced acute kidney injury.Renal failure · 2025Article
- Renoprotective Effects of Phloretin and TUDCA via Simultaneous Inhibition of TLR4/MyD88/NF-κB and BiP/PERK/CHOP Pathways in AKI Under Diabetic Condition.Applied biochemistry and biotechnology · 2025Article
- Dysregulation and gene polymorphisms of Vitamin D receptor: its implications in lipid metabolic disorders.Molecular biology reports · 2025Review
- Protective role of vitamin D receptor against mitochondrial calcium overload from PMRedox biology · 2025Article
- Ebselen Alleviates Sepsis-Induced Acute Kidney Injury by Regulating Endoplasmic Reticulum Stress, Apoptosis, and Oxidative Stress.Veterinary medicine and science · 2025Article
- Identification of Ferroptosis-Related Genes in Patients with Renal Ischemia-Reperfusion Injury.International journal of general medicine · 2025Article
- Article
- Identification of Hub Genes for Dexmedetomidine Alleviation of Limb Ischemia-Reperfusion-Induced Lung Injury in Rats by Transcriptomic.Journal of inflammation research · 2025Article
- Paricalcitol alleviates intestinal ischemia-reperfusion injury via inhibition of the ATF4-CHOP pathway.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activating transcription factor 4 (ATF4) is one of the key effectors of endoplasmic reticulum stress (ERS), ATF4/CHOP pathway-mediated ERS plays an important role in the progression of acute kidney disease (AKI). We have previously reported that Vitamin D receptor (VDR) exert renoprotection in rodent AKI models. However, whether ATF4, as well as ERS, is involved in the protective effect of VDR in ischemia-reperfusion (I/R) induced AKI is unknown. Herein, we showed that VDR agonist paricalcitol and VDR overexpression alleviated I/R-induced renal injury and cells apoptosis with decreased ATF4 and attenuated ERS, while VDR deletion significantly resulted in further increased ATF4, more drastic ERS and renal injury in I/R mice models. In addition, paricalcitol remarkably reduced Tunicamycin (TM) induced ATF4 and ERS with attenuated renal injury, while VDR deletion aggravated the above changes in TM mice models. Moreover, overexpression of ATF4 partially abolished the effect of paricalcitol against TM-induced ERS and apoptosis, while inhibition of ATF4 enhanced the protective effect of paricalcitol. Bioinformatics analysis indicated potential VDR binding sites on ATF4 promotor sequence which were further confirmed by ChIP-qPCR and dual-luciferase reporter gene assay. In conclusion, VDR attenuated I/R-induced AKI by suppressing ERS partly via transcriptional regulation of ATF4.
Identifiers
What OpenQuestion holds
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.