ReviewInternational journal of molecular medicine2026
Epigenetic regulation in a high-sugar environment (Review).
Review in International journal of molecular 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.
- Long non-coding RNAs in the crosstalk between diabetes and colorectal cancer: molecular mechanisms and endocrine pathways.Frontiers in molecular biosciences · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prevalence of diabetes and its complications has become a major global health challenge, with its pathological process closely linked to the phenomenon of 'metabolic memory' induced by persistent hyperglycemia. Epigenetic regulation is recognized as the core molecular mechanism underpinning this process. The present review systematically elucidated how the hyperglycemic microenvironment profoundly regulates cellular functions and drives the onset and progression of diabetes and its vascular complications by reprogramming three major epigenetic pathways: DNA methylation, histone modifications and non‑coding RNA expression. The present review elaborated in detail how high glucose induces alterations in the DNA methylation status of specific genes (such as PDX1 and CXCR4) within key target cells including pancreatic β‑cells, hepatocytes, muscle cells and adipocytes; how it modulates multiple histone modifications, including emerging histone lactylation (such as H3K18la), thereby directly activating pathogenic gene transcription; and how it disrupts non‑coding) RNA networks (such as long non‑coding RNA MALAT1 and microRNA 21) to mediate inflammation, oxidative stress and fibrosis by interfering with signaling pathways such as PI3K/Akt and TGF‑β. Furthermore, the present review specifically emphasized the cellular and tissue specificity of high‑glucose‑induced epigenetic regulation, thereby elucidating its unique mode of action in specific complications such as diabetic nephropathy and cardiovascular disease. Finally, the present review considered the substantial potential of targeting key epigenetic enzymes (such as DNA methyltransferases, histone deacetylases) or using epigenetic markers as biomarkers and novel therapeutic strategies. This provides a conceptual framework and directions for ultimately 'eradicating' metabolic memory and achieving precise prevention and treatment of diabetes and its complications.
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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.