ReviewJournal of inflammation research2025
Epigenetic Modulation by Lactylation in Sepsis: Linking Metabolism to Immune Dysfunction.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Research on Sepsis and Metabolic Reprogramming from 1998 to 2025: A Bibliometric and Visualized Analysis.Shock (Augusta, Ga.) · 2026Article
- A Novel Approach to Neuropathic Pain Treatment: Lactylation Targeting Microglia.Molecular neurobiology · 2026Review
- Brain endothelial PTPRO drives LPS-induced metabolic reprogramming and neuroinflammation in sepsis-associated encephalopathy.Journal of neuroinflammation · 2026Article
- Sepsis and the immunometabolic inflammatory response.npj metabolic health and disease · 2026Review
- Jaceosidin Attenuates Sepsis-Induced Myocardial Dysfunction by Promoting SIRT2-Mediated Inhibition of Histone H3K18 Lactylation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Shengmai Injection as adjunctive therapy in sepsis and septic shock: a retrospective cohort study.Frontiers in cellular and infection microbiology · 2026Article
- Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026Review
- Macrophage reprogramming and functional plasticity in sepsis.Frontiers in immunology · 2026Review
- Lactate and lactylation in sepsis: regulation of immune-metabolic crosstalk and organ injury.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lactate, traditionally viewed as a metabolic byproduct, is now recognized as a key regulator of immune and epigenetic processes in sepsis. A recently discovered post-translational modification, lactylation, utilizes lactate as a substrate and plays a crucial role in cellular regulation. Accumulating evidence suggests that elevated lactate levels contribute to immune dysfunction in sepsis by modulating the activity of various immune cells. This modification links metabolic changes to immune regulation, making it a crucial factor in sepsis progression. Understanding how lactylation is altered in sepsis unveils critical links between immunometabolism, epigenetic regulation, and disease pathophysiology. These insights also highlight the interplay between metabolic and epigenetic reprogramming during septic progression. As a result, lactylation has emerged as a promising biomarker and potential therapeutic target in sepsis. This review aims to summarize the latest findings on lactate metabolism, lactylation modifications, and their immunometabolic implications in sepsis.
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.