Evidence map›Paper›PMID 42813062›Full record

ReviewFrontiers in immunology2026

Glycolytic reprogramming and cell-specific lactylation in asthma: an evidence-graded framework for testable metabolic-epigenetic profiles.

Shu Li, Haoxiang Fang, Kun Wang

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Shu LiThe First Clinical Medical College of Anhui University of Chinese Medicine, Hefei, China.
Haoxiang FangThe First Clinical Medical College of Anhui University of Chinese Medicine, Hefei, China.
Kun WangHuixue Research Center, Anhui University of Chinese Medicine, Hefei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is metabolically heterogeneous, but existing syntheses often place patient observations, animal perturbations, cross-disease mechanisms, and therapeutic concepts on the same evidentiary plane. This review addresses that problem by organizing glycolytic reprogramming and lysine lactylation through a three-tier hierarchy: human asthma observations, mechanistic perturbation in asthma-relevant models, and cross-disease or conceptual precedents. Mitochondrial and redox disturbances alter glycolytic and oxidative capacity across immune and structural cells, whereas lactate can function separately as an exported acidifying metabolite and as an intracellular substrate for site-specific lactylation. Four asthma-associated circuits have the strongest direct mechanistic support: epithelial histone H3 lysine 18 lactylation (H3K18la)-colony-stimulating factor 1 receptor (CSF1R) signaling; cluster of differentiation 4-positive (CD4

Indexed as

AsthmaEpigenesis, GeneticGlycolysisAnimalsHistonesHumansMetabolic ReprogrammingHistonesasthmachromatin regulationglycolytic reprogrammingimmunometabolismlysine lactylation

Identifiers

PMID42813062
PMCPMC13621785

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.