Overlapping roles of dysregulated glycolysis in the pathophysiology of diabetes and cancer

Clicks: 8
ID: 337618
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #224 of 226 articles by views in endocrine reviews

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 226 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
Emerging evidence highlights a strong association between type 2 diabetes (T2D) and increased cancer risk, with partially overlapping metabolic disruptions potentially driving both diseases. Chronic hyperglycemia, a hallmark of T2D, disrupts glycolytic flux and contributes to the accumulation of toxic intermediates, driving cellular damage and diabetic complications. Specifically, dysregulation of glycolytic enzymes diverts metabolites into harmful pathways, promoting oxidative and glycative stress across multiple cell types. Similar metabolic disturbances support cancer development and progression by fueling rapid tumor cell proliferation. This review explores the role of abnormal glycolysis as a potential mechanistic link between T2D and cancer, detailing shared enzymatic alterations and metabolic pathway shifts. Additionally, it discusses pharmacological therapeutic strategies targeting glycolysis-related abnormalities common to both diseases, emphasizing the need for balanced metabolic modulation.
Reference Key
openalex_W7224112181 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors
Journal endocrine reviews
Year 2026
DOI
10.1210/endrev/bnag043
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.