ArticleFrontiers in immunology2026
Lactylation-driven PDLIM1/PDAP1 axis remodels the inflammatory landscape of acute lung injury: mechanistic insights and precision intervention.
Article in Frontiers in immunology, 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.
- Multiomics Mendelian Randomization Identifies Lactylation-Related Molecular Traits in Type 1 Diabetes.Journal of diabetes research · 2026Article
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
Introduction: Acute lung injury (ALI) remains a lethal clinical challenge driven by an uncontrolled "cytokine storm" resulting from dysregulated inflammatory networks. The metabolic and molecular mechanisms orchestrating this process remain incompletely understood. Methods: We integrated multi-omics profiling with functional analyses in murine models and human iPSC-derived alveolar organoids. Key molecular players were identified through loss-of-function and pharmacological interventions, and the effects of a dual-target strategy using progesterone (PT) and ethyl methanesulfonate (EMS) were evaluated. Results: Metabolic reprogramming-driven lactylation emerged as a central orchestrator of inflammatory progression. PDAP1 lactylation acts as a pivotal metabolic switch for NLRP3 inflammasome activation and selective IL-1β release. Functional deficiency of PDLIM1 releases the molecular brake on NF-κB signaling, precipitating a broad-spectrum inflammatory cascade. These modifications bridge metabolic stress with oxidative damage via the NRF2/GPX4-mediated ferroptotic pathway. The "dual-target, dual-drug" intervention-PT targeting the PDLIM1 axis and EMS selectively disrupting PDAP1-mediated IL-1β maturation-effectively quelled systemic inflammation and attenuated ALI pathology in both in vivo and organoid models. Discussion: This study elucidates a novel metabolic-immune coupling mechanism in pulmonary polarization, shifting the focus from pan-inflammatory suppression toward precision immunomodulation. The findings provide a transformative theoretical paradigm for the management of ALI.
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.