ReviewDiabetology international2025
Pathophysiological hallmarks in type 2 diabetes heterogeneity (review).
Review in Diabetology international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- Impact of a remote nutrition education on low-carbohydrate diet based in type 2 diabetes management: findings from a Brazilian primary care randomized controlled trial.Diabetology international · 2026Article
- Reduced circulating Mig-6 levels are associated with dysglycemia in metabolic dysfunction associated steatotic liver disease (MASLD).BMJ open diabetes research & care · 2026Article
- Cluster-specific genetic associations of CDKAL1, CDKN2A, CDKN2B, HHEX, KCNQ1, MTNR1B, PAX4, SLC30A8, TCF7L2, and UBE2E2 variants in new onset type 2 diabetes.Scientific reports · 2025Article
- Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanistic complexity in type 2 diabetes (T2DM) is primarily responsible for the degrees of heterogeneity and development of complications. A complex mode of interactions between different pathophysiological events and diabetogenic environmental factors support for the genesis of diabetes heterogeneity both in phenotypic and clinical contexts. The currently used diabetes classification strategies suffer from several inconsistencies that cannot fully capture the inherent heterogeneity among the diabetes patients. To effectively address this pathobiological and heterogeneity-related issue in diabetes research, the current review proposes nine pathophysiological hallmarks of T2DM that aims to mechanistically explain complexities of diabetes associated pathophysiological events and their underlying features. These pathophysiological hallmarks are pancreatic beta cell dysfunction, insulin sensitivity, insulin resistance, obesity, aging, subclinical inflammation, metabolic dysregulation, prothrombotic state induction and hypertension. Detail knowledge of these pathophysiological hallmarks with their key molecular mediators, influencing factors, clinical biomarkers and clinical assessment methodologies will greatly support precision medicine approaches in diabetes including patient stratification, subtype diagnosis and treatment. Supplementary Information: The online version contains supplementary material available at 10.1007/s13340-024-00783-w.
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Registered trials
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