ArticleRedox biology2019
Inhibition of Brd4 alleviates renal ischemia/reperfusion injury-induced apoptosis and endoplasmic reticulum stress by blocking FoxO4-mediated oxidative stress.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
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Who cites it
145 citing papers in PubMed, 242 citations in OpenAlex.
- Ginsenoside Rg1 ameliorates renal ischemia-reperfusion injury by inhibiting FABP1-regulated Nrf2/HO-1 pathway.Renal failure · 2026Article
- GADD45A may be a potential biomarker associated with endoplasmic reticulum stress in focal segmental glomerulosclerosis.Biochemistry and biophysics reports · 2026Article
- SIRT7-mediated desuccinylation of FOXO4 suppresses ferroptosis to alleviate LPS-induced acute lung injury.Redox biology · 2026Article
- Targeting bromodomain and extraterminal proteins in cardiovascular disease: Pathological mechanisms and therapeutic applications.The Journal of international medical research · 2026Review
- Sophocarpine Alleviates Renal Ischemia-Reperfusion Injury by Mitigating Oxidative Stress and Mitochondrial Dysfunction via the SIRT1/PGC-1α Axis.Biomedicines · 2026Article
- BRD4 Inhibition alleviates sepsis-associated acute kidney injury via suppression of NOX4-mediated oxidative stress and inflammation.Cell death discovery · 2026Article
- Blocking FOXO4 confers neuroprotection against oxidative stress and ischemia-reperfusion caused neuronal injury.Journal of neuropathology and experimental neurology · 2026Article
- Brazilin attenuates kidney ischemia-reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction.Histology and histopathology · 2026Article
- Ferulic Acid Alleviates Chemotherapy-Induced POI by Targeting the Grp78 and Perk-eIF2α-ATF4-CHOP Pathway to Attenuate Endoplasmic Reticulum Stress.Biomedicines · 2026Article
- Disrupting FOXO4 function confers neuroprotection against oxidative stress and ischemia-reperfusion-caused neuronal injury.bioRxiv : the preprint server for biology · 2026Article
- Selenium-doped carbon dots nanozymes hitchhiking tailored liposomes block neuronal pyroptosis through GPX4/ROS/NLRP3/GSDMD axis to attenuate ischemic stroke.Journal of nanobiotechnology · 2026Article
- 17-β-Estradiol Protects Chondrocytes From Senescence and Ameliorates Osteoarthritis Progression via ERα-AKT-FOXO4 Pathway.Journal of cellular and molecular medicine · 2026Article
- Integrative epigenomic and transcriptomic profiling reveals organ-specific and coordinated cold stress responses in the brain and gill of Nile tilapia.Stress biology · 2026Article
- Apoptosis, Pyroptosis, and Necroptosis (PANoptosis) may be Present in Renal Ischemic Injury.Current medicinal chemistry · 2026Article
- ROS-responsive graphene-hyaluronic acid nanomedicine for targeted therapy in renal ischemia/reperfusion injury.Theranostics · 2026Article
- Imidazole Propionate Induces Kidney Damage by Activating the ROS-NLRP3 Signaling Pathway Through mTOR Inhibition of Autophagy in Renal Tubular Epithelial Cells.Mediators of inflammation · 2026Article
- Tangzhiqing enhances glucose and lipid metabolism in obese diabetic rats by targeting PI3K/AKT and ER stress.Frontiers in veterinary science · 2026Article
- Fecal microbiota transplantation ameliorates radiation-induced lung injury by reshaping gut metabolic homeostasis to activate FAM134B-mediated ER-phagy.PLoS pathogens · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- FOXO4 Facilitates Diabetic Retinopathy by Mediating KLF7 Transcription and Affecting the TLR4/MyD88/NF-κB Pathway.Applied biochemistry and biotechnology · 2026Article
85 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia/reperfusion injury (I/R) is one of the leading causes of acute kidney injury (AKI) that typically occurs in renal surgeries. However, renal I/R still currently lacks effective therapeutic targets. In this study, we proved that inhibition of Brd4 with its selective inhibitor, JQ1, could exert a protective role in renal I/R injury in mice. Inhibiting Brd4 with either JQ1 or genetic knockdown resulted in reduction of endoplasmic reticulum stress (ERS)-associated protein and proapoptotic protein expression both in I/R-induced injury and hypoxia/reoxygenation (H/R) stimulation in HK-2 cells. H/R-induced apoptosis and ERS depended on oxidative stress in vitro. Moreover, FoxO4, which is involved in the generation of hydrogen peroxide, was up-regulated during H/R stimulation-mediated apoptosis and ERS, and this upregulation could be abolished by Brd4 inhibition. Consistently, FoxO4-mediated ROS generation was attenuated upon inhibition of Brd4 with JQ1 or siRNA against Brd4. Further, the transcriptional activity of FoxO4 was suppressed by PI3K and AKT phosphorylation, which are upstream signals of FoxO4 expression, and were enhanced by Brd4 both in vivo and in vitro. In conclusion, our results proved that Brd4 inhibition blocked renal apoptotic and ERS protein expression by preventing FoxO4-dependent ROS generation through the PI3K/AKT pathway, indicating that Brd4 could be a potential therapeutic target for renal I/R injury.
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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.