ReviewJournal of translational medicine2026
Lactylation in tissue fibrosis: epigenetic mechanisms, metabolic crosstalk, and therapeutic opportunities.
Review in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Histone modifications in skin fibrosis: linking immune dysregulation, metabolic reprogramming, and persistent fibrotic remodeling.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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTissue fibrosis, driven by chronic inflammation and degeneration, leads to progressive organ dysfunction. While significant advancements have been made, effective therapies remain limited. Lactylation, a newly recognized post-translational modification (PTM), has attracted attention in cellular regulation. However, the precise mechanisms through which lactylation influences fibrosis remain poorly understood. MAIN BODY: In this Review, we integrate current insights into the origin, molecular mechanisms, and dynamic regulation of both histone and non-histone lactylation, with a particular focus on its mechanistic roles in tissue fibrosis. Lactylation acts as a metabolic-epigenetic interface, linking altered cellular metabolism to chromatin remodeling, transcriptional reprogramming, and activation of fibrosis-related signaling networks. Through these processes, lactylation exerts context-dependent and organ-specific effects in fibrotic diseases of the liver, kidney, lung, skin, and other tissues. Notably, its regulatory influence extends beyond non-malignant fibrotic conditions to encompass tumor-associated stromal fibrosis and fibrogenic remodeling during post-injury tissue repair. Moreover, this Review highlights the therapeutic potential of targeting both histone and non-histone lactylation in fibrosis and explores its crosstalk with other PTMs, including acetylation and methylation.
conclusionLactylation represents a critical metabolic-epigenetic axis in the initiation and progression of tissue fibrosis. Targeting lactylation-either by modulating specific lactylation sites or regulating lactatemetabolizing key enzymes-offers an effective approach to suppress fibrosis progression and provides a foundation for the development of precision antifibrotic therapies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.