ReviewNeuroscience bulletin2026
Unveiling the "Glycolysis-Lactate-Lactylation" Axis: A Novel Target in Ischemic Cerebrovascular Disease.
Review in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Metabolic-epigenetic crosstalk in latent autoimmune diabetes in adults: potential roles of lactate-induced histone lactylation in immune regulation and pancreatic β-cell fate.Frontiers in endocrinology · 2026Review
- Inflammation-centered neurovascular-immune-metabolic remodeling in ischemic stroke: stage-dependent mechanisms, regulated cell death, and therapeutic translation.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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic cerebrovascular disease involves complex interactions between metabolic reprogramming and epigenetic regulation. Recent studies indicate that enhanced glycolysis and lactate accumulation under hypoxic conditions not only maintain cell viability by supplying energy but also participate in disease regulation through lactylation. Lactylation regulates gene expression, immune polarization, metabolic enzyme activity, and angiogenesis through epigenetic remodeling. In ischemic cerebrovascular disease, lactylation exerts dual roles: on one hand, it can induce neuronal death, exacerbate neuroinflammation, and form a vicious metabolic cycle; on the other hand, it can influence immune cell function and gene expression, thereby exerting neuroprotective effects. Accordingly, targeting lactate metabolism or lactylation-modifying enzymes holds considerable therapeutic potential. Nevertheless, the spatiotemporal regulation, synergistic effects, and broader physiopathological implications of lactylation warrant further in-depth investigation. This review systematically summarizes the role of the "glycolysis-lactate-lactylation" axis in the pathogenesis of ischemic cerebrovascular disease, and discusses its potential as a therapeutic target.
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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.