ArticleRedox biology2018
Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 260 papers, 2 of them syntheses that pooled it.
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Who cites it
260 citing papers in PubMed, 2 syntheses or guidelines pooled it, 452 citations in OpenAlex.
- Mitochondrial Dysfunction in Individuals with Diabetic Kidney Disease: A Systematic Review.Cells · 2022Pooled it
- Role of ROS-Induced NLRP3 Inflammasome Activation in the Formation of Calcium Oxalate Nephrolithiasis.Frontiers in immunology · 2022Pooled it
- Hirsutine mitigates high glucose-induced cell injuryRenal failure · 2026Article
- Metabolic reprogramming in diabetic panvascular disease: Molecular mechanism and therapeutic strategies.iScience · 2026Review
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- Liver-to-kidney apolipoprotein J trans-accumulation exacerbates diabetic renal injury by disrupting TFEB-mediated lipid homeostasis.Diabetologia · 2026Article
- Curcumin attenuates high glucose-induced apoptosis in renal tubular epithelial cells by enhancing the Nrf2/heme oxygenase-1 antioxidant pathway.World journal of nephrology · 2026Article
- ZFP36-ferroptosis axis as a key renal protective pathway in diabetic kidney disease.Endocrine journal · 2026Article
- Review
- Advances in understanding the NLRP3 inflammasome‑mediated mechanisms and therapeutic targets in diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- Inflammasome activation dictates the efficacy of antimycobacterial activity of frontline TB drugs.PLoS pathogens · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Tissue-Specific Transcriptomic Profiling of Vitamin-Dependent Mitochondrial Pathways in Female Buffalo.Cell biochemistry and biophysics · 2026Article
- NDUFA5 deficiency promotes renal inflammation in diabetic nephropathy via mitochondrial ROS signaling.iScience · 2026Article
- Histone H3K9 lactylation activates the TXNIP/NLRP3 pathway to drive macrophage inflammation after spinal cord injury.Redox biology · 2026Article
- Abnormal lipid metabolism in senescent renal tubular cells in diabetic nephropathy.Cellular and molecular life sciences : CMLS · 2026Review
- PDK4 drives abdominal aortic aneurysm by promoting smooth muscle cell metabolic reprogramming and NLRP3-mediated pyroptosis.Nature communications · 2026Article
- Targeting SAT1 alleviates high glucose-induced tubular ferroptosis and fibrosis: implications for diabetic kidney disease.Histochemistry and cell biology · 2026Article
- PKM2 from hyperactive neuron aggravate lung injury post-stroke by promoting FOXO3A/TXNIP mitochondria translocation in mice.Redox biology · 2026Article
- Thioredoxin protects against diabetic hearing loss by regulating TOMM22 mediated mitochondrial autophagy in hair cells and inhibiting microglial M1 polarization.Scientific reports · 2026Article
200 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
NLRP3/IL-1β activation via thioredoxin (TRX)/thioredoxin-interacting protein (TXNIP) following mitochondria ROS (mtROS) overproduction plays a key role in inflammation. However, the involvement of this process in tubular damage in the kidneys of patients with diabetic nephropathy (DN) is unclear. Here, we demonstrated that mtROS overproduction is accompanied by decreases in TRX expression and TXNIP up-regulation. In addition, we discovered that mtROS overproduction is also associated with increases in NLRP3/IL-1β and TGF-β expression in the kidneys of patients with DN and db/db mice. We reversed these changes in db/db mice by administering a peritoneal injection of MitoQ, an antioxidant targeting mtROS. Similar results were observed in human tubular HK-2 cells subjected to high-glucose (HG) conditions and treated with MitoQ. Treating HK-2 cells with MitoQ suppressed the dissociation of TRX from TXNIP and subsequently blocked the interaction between TXNIP and NLRP3, leading to the inhibition of NLRP3 inflammasome activation and IL-1β maturation. The effects of MitoQ were enhanced by pretreatment with TXNIP siRNA and abolished by pretreatment with monosodium urate (MSU) and TRX siRNA in vitro. These results suggest that mitochondrial ROS-TXNIP/NLRP3/IL-1β axis activation is responsible for tubular oxidative injury, which can be ameliorated by MitoQ via the inhibition of mtROS overproduction.
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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.