ArticleMolecular cell2014
Nrf2 amplifies oxidative stress via induction of Klf9.
Article in Molecular cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
137 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- Antioxidant therapy for treatment of inflammatory bowel disease: Does it work?Redox biology · 2015Pooled it
- Transcriptional factor KLF9 in pulmonary fibrosis: from molecular mechanisms to precision intervention-a narrative review.Journal of thoracic disease · 2026Review
- Nrf2 promotes NLRP3 inflammasome assembly and activation by Klf9-TXNIP axis.Cell death discovery · 2026Article
- Genetic and transcriptomic signatures of host control in HIV-1 infection.Retrovirology · 2026Article
- KLF9 Aggravates Doxorubicin-Induced Cardiotoxicity by Regulating the ROS/p53 Signalling Pathway.Cardiovascular toxicology · 2026Article
- IGFBP3 repression driven by inflammation links air pollution to placental and developmental defects.EMBO molecular medicine · 2026Article
- Loss of Peroxiredoxin 6 Drives Age-Related Klf9/NF-Antioxidants (Basel, Switzerland) · 2026Article
- Aging, oxidative stress, and cataracts: Therapeutic prospects and translational insights into peroxiredoxin 6.Progress in retinal and eye research · 2026Review
- Spatial and Single-Cell Transcriptomics Reveal Keratinocytes as Key Players in Vulvar Lichen Sclerosus Pathogenesis.The Journal of investigative dermatology · 2026Article
- Environmental Exposures and Oxidative Stress in Retinal and Optic Nerve Diseases: Mechanisms, Consequences, and Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2026Review
- Impact of reactive oxygen species on bone regeneration in diabetes: Mechanisms and therapeutic strategies.Redox biology · 2025Review
- Review
- Gene expression responses revealing immune mechanisms in tambaqui (Colossoma macropomum) during the early phase of acute Flavobacterium oreochromis infection.Molecular biology reports · 2025Article
- Topical Instillation of N-Acetylcysteine and N-Acetylcysteine Amide Impedes Age-Related Lens Opacity in Mice.Biomolecules · 2025Article
- Gene expression profiles in respiratory settings in rats under extracorporeal membrane oxygenation.Journal of thoracic disease · 2025Article
- Nrf1 acts as a highly-conserved determinon for maintaining robust redox homeostasis in the eco-evo-devo process of life histories.Cell stress · 2025Review
- Krüppel-like factors in mitochondrial quality control.Frontiers in physiology · 2025Review
- The tumor microenvironment: adding pieces to the puzzle.Frontiers in immunology · 2025Review
- Glycolysis in Peritubular Endothelial Cells and Microvascular Rarefaction in CKD.Journal of the American Society of Nephrology : JASN · 2025Article
- Gold nanorod-based engineered nanogels for cascade-amplifying photothermo-enzymatic synergistic therapy.Journal of pharmaceutical analysis · 2024Article
77 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) activate NF-E2-related transcription factor 2 (Nrf2), a key transcriptional regulator driving antioxidant gene expression and protection from oxidant injury. Here, we report that in response to elevation of intracellular ROS above a critical threshold, Nrf2 stimulates expression of transcription Kruppel-like factor 9 (Klf9), resulting in further Klf9-dependent increases in ROS and subsequent cell death. We demonstrated that Klf9 independently causes increased ROS levels in various types of cultured cells and in mouse tissues and is required for pathogenesis of bleomycin-induced pulmonary fibrosis in mice. Mechanistically, Klf9 binds to the promoters and alters the expression of several genes involved in the metabolism of ROS, including suppression of thioredoxin reductase 2, an enzyme participating in ROS clearance. Our data reveal an Nrf2-dependent feedforward regulation of ROS and identify Klf9 as a ubiquitous regulator of oxidative stress and lung injury.
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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.