ArticleNature communications2023
N
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 56 citations in OpenAlex.
- A multistage micro-nano biosystem prevents sepsis-associated encephalopathy through coordinated neuroinflammation suppression and gut-brain axis modulation.Bioactive materials · 2026Article
- Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026Review
- METTL7B Expression in Sepsis: Association With Disease Severity and 28-Day Mortality.Journal of clinical laboratory analysis · 2026Article
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- mRedox biology · 2026Review
- Review
- RNA modification-mediated multidimensional crosstalk: a novel perspective on gene expression regulation.Genome biology · 2026Review
- Brain-wide mapping of oligodendrocyte organization, oligodendrogenesis, and myelin injury.Cell · 2026Article
- ALKBH5-Driven m6A Demethylation Boosts Inflammation and Autophagy in LPS-Stimulated Macrophages.Immunity, inflammation and disease · 2026Article
- Multi-cohort transcriptomics integration for building and validating a diagnostic model of peripheral blood septic shock.Frontiers in immunology · 2026Article
- m6A RNA methylation in sepsis-induced cardiomyopathy: direct cardiac mechanisms, emerging therapeutic targets, and translational gaps.Frontiers in medicine · 2026Review
- Phenylacetylglutamine exacerbates sepsis-induced cardiac dysfunction and left ventricular remodeling via the ferroptosis and TLR4/NF-κB pathway.Frontiers in cardiovascular medicine · 2026Article
- ADAP-METTL3 modulates the inflammatory responses of macrophages via mCell death & disease · 2025Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- Impact of N-acetyltransferase 10 on macrophage activation and inflammation-induced cardiac dysfunction.Cell death & disease · 2025Article
- FTO deficiency facilitates epithelia dysfunction in oral lichen planus.Molecular therapy. Nucleic acids · 2025Article
- eIF3a function in immunity and protection against severe sepsis by regulating B cell quantity and function through mActa pharmaceutica Sinica. B · 2025Article
- Sepsis-induced cardiomyopathy: understanding pathophysiology and clinical implications.Archives of toxicology · 2025Review
- Lactylation of Histone H3k18 and Egr1 Promotes Endothelial Glycocalyx Degradation in Sepsis-Induced Acute Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacteria-triggered sepsis is characterized by systemic, uncontrolled inflammation in affected individuals. Controlling the excessive production of pro-inflammatory cytokines and subsequent organ dysfunction in sepsis remains challenging. Here, we demonstrate that Spi2a upregulation in lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages reduces the production of pro-inflammatory cytokines and myocardial impairment. In addition, exposure to LPS upregulates the lysine acetyltransferase, KAT2B, to promote METTL14 protein stability through acetylation at K398, leading to the increased m
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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.