ArticleCell death & disease2023
DUSP1 protects against ischemic acute kidney injury through stabilizing mtDNA via interaction with JNK.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 65 citations in OpenAlex.
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- Mitochondrial dysfunction of renal tubular epithelial cells in chronic kidney disease-associated fibrosis: from organelle homeostasis to multicellular remodeling.Molecular biology reports · 2026Review
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Sophocarpine Alleviates Renal Ischemia-Reperfusion Injury by Mitigating Oxidative Stress and Mitochondrial Dysfunction via the SIRT1/PGC-1α Axis.Biomedicines · 2026Article
- Ogg1 regulates TGF‑β-Smad3 signalling and fibrosis progression in chronic kidney disease.Communications biology · 2026Article
- Comprehensive analysis of RNA sequencing reveals DNA damage response and immune-associated alternative splicing and RBP regulators contributing to preeclampsia.BMC genomics · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- DUSP26 protects against acute kidney injury by dephosphorylating p53 at serine 312.Nature communications · 2026Article
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- IKBKE downregulation increases chemosensitivity through pyroptosis mediated by the caspase-3/GSDME pathway in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- DUSP1 Attenuates Renal Injury in Diabetic Nephropathy by Modulating Ferroptosis: Evidence From Animal Experiments.Immunity, inflammation and disease · 2026Article
- cGAS-STING pathway in innate immunity and its cell-specific role in kidney diseases.Frontiers in immunology · 2026Review
- Mitochondrial dysfunction in sepsis-associated acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- STING activation in renal and prostatic inflammation: potential therapeutic targets and immune regulation.Frontiers in immunology · 2026Review
- Machine learning and transcriptomic analysis identify tubular injury biomarkers in patients with chronic kidney disease.International urology and nephrology · 2025Article
- Identification of diagnostic biomarkers and mitochondrial metabolic characteristics in sepsis-associated acute kidney injury.European journal of medical research · 2025Article
- A novel ligustrazine-based nanodelivery system protects against doxorubicin-induced cardiotoxicity by targeting the SIRT5-DUSP1 axis for mitochondrial repair.Journal of nanobiotechnology · 2025Article
- Hesperetin ameliorates mitochondrial dysfunction in acute kidney injury by mediating autophagy and inhibiting the cGAS-STING pathway.Journal of molecular histology · 2025Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism underlying acute kidney injury (AKI) and AKI-to-Chronic kidney disease (CKD) transition remains unclear, but mitochondrial dysfunction may be a key driving factor. Literature reports suggest that dual-specificity phosphatase 1 (DUSP1) plays a critical role in maintaining mitochondrial function and structural integrity. In this study, ischemic Acute Kidney Injury (AKI) and post-ischemic fibrosis models were established by clamping the renal pedicle with different reperfusion times. To investigate the role of DUSP1, constitutional Dusp1 knockout mice and tubular-specific Sting knockout mice were used. Mitochondrial damage was assessed through electron microscopy observation, measurements of mitochondrial membrane potential, mtDNA release, and BAX translocation. We found that Dusp1 expression was significantly upregulated in human transplant kidney tissue and mouse AKI tissue. Dusp1 gene deletion exacerbated acute ischemic injury, post-ischemic renal fibrosis, and tubular mitochondrial dysfunction in mice. Mechanistically, DUSP1 could directly bind to JNK, and DUSP1 deficiency could lead to aberrant phosphorylation of JNK and BAX mitochondria translocation. BAX translocation promoted mitochondrial DNA (mtDNA) leakage and activated the cGAS-STING pathway. Inhibition of JNK or BAX could inhibit mtDNA leakage. Furthermore, STING knockout or JNK inhibition could significantly mitigate the adverse effects of DUSP1 deficiency in ischemic AKI model. Collectively, our findings suggest that DUSP1 is a regulator for the protective response during AKI. DUSP1 protects against AKI by preventing BAX-induced mtDNA leakage and blocking excessive activation of the cGAS-STING signaling axis through JNK dephosphorylation.
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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 Socratic graph.