ArticleNature immunology2013
Suppression of inflammation and acute lung injury by Miz1 via repression of C/EBP-δ.
Article in Nature immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 54 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
54 citing papers in PubMed, 87 citations in OpenAlex.
- Unraveling Novel Strategies: Targeting Miz1 for Degradation to Enhance Antiviral Defense against Influenza A Virus.Journal of respiratory biology and translational medicine · 2024Article
- Miz1 represses type I interferon production and limits viral clearance during influenza A virus infection.Science signaling · 2024Article
- Network Pharmacology Analysis of the Therapeutic Potential of Colchicine in Acute Lung Injury.International journal of clinical practice · 2024Article
- ACE2 in chronic disease and COVID-19: gene regulation and post-translational modification.Journal of biomedical science · 2023Review
- Miz1 promotes KRAS-driven lung tumorigenesis by repressing the protocadherin Pcdh10.Cancer letters · 2023Article
- Protective effects of Pudilan Tablets against osteoarthritis in mice induced by monosodium iodoacetate.Scientific reports · 2023Article
- STV-Na attenuates lipopolysaccharide-induced lung injury in mice via the TLR4/NF-kB pathway.Immunity, inflammation and disease · 2023Article
- Suppression of Allergic Asthma by Loss of Function of Miz1-mediated Th1 Skewing.American journal of respiratory cell and molecular biology · 2022Article
- CEBPD modulates the airway smooth muscle transcriptomic response to glucocorticoids.Respiratory research · 2022Article
- FGF1 alleviates LPS-induced acute lung injury via suppression of inflammation and oxidative stress.Molecular medicine (Cambridge, Mass.) · 2022Article
- Severe acute respiratory syndrome coronavirus 2 causes lung inflammation and injury.Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2022Review
- CCAAT/Enhancer-Binding Proteins in Fibrosis: Complex Roles Beyond Conventional Understanding.Research (Washington, D.C.) · 2022Review
- Article
- The small RNA mascRNA differentially regulates TLR-induced proinflammatory and antiviral responses.JCI insight · 2021Article
- Anti-inflammatory effects of microRNA-223 on sepsis-induced lung injury in rats by targeting the Toll-like receptor signaling pathway.Experimental and therapeutic medicine · 2021Article
- Overexpression of Limb Bud and Heart Alleviates Sepsis-Induced Acute Lung Injury via Inhibiting the NLRP3 Inflammasome.BioMed research international · 2021Article
- miR-221-5p-Mediated Downregulation of JNK2 Aggravates Acute Lung Injury.Frontiers in immunology · 2021Article
- Common Polymorphisms in theFrontiers in cardiovascular medicine · 2021Article
- Identification of the SARS-CoV-2 Entry Receptor ACE2 as a Direct Target for Transcriptional Repression by Miz1.Frontiers in immunology · 2021Article
- Epithelial cell-specific loss of function ofScience advances · 2020Article
Corrections and comments
- Retraction · 2025-01-07Concerns/Issues about Data · Falsification/Fabrication of Data · Investigation by Company/Institution · Investigation by Journal/Publisher · Objections by Author(s) ·
- Retracted
Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
Abstract
Inflammation is essential for host defense but can cause tissue damage and organ failure if unchecked. How the inflammation is resolved remains elusive. Here we report that the transcription factor Miz1 was required for terminating lipopolysaccharide (LPS)-induced inflammation. Genetic disruption of the Miz1 POZ domain, which is essential for the transactivation or repression activity of Miz1, resulted in hyperinflammation, lung injury and greater mortality in LPS-treated mice but a lower bacterial load and mortality in mice with Pseudomonas aeruginosa pneumonia. Loss of the Miz1 POZ domain prolonged the expression of proinflammatory cytokines. After stimulation, Miz1 was phosphorylated at Ser178, which was required for recruitment of the histone deacetylase HDAC1 to repress transcription of the gene encoding C/EBP-δ, an amplifier of inflammation. Our data provide a long-sought mechanism underlying the resolution of LPS-induced inflammation.
Indexed as
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.