ReviewCureus2026
Advanced Glycation End Products and Genetic Polymorphism in the Pathogenesis of Microvascular Complications in Type 2 Diabetes Mellitus: A Narrative Review.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with type 2 diabetes mellitus often experience microvascular complications, including diabetic retinopathy, nephropathy, and neuropathy. Despite advances in glucose-lowering treatments, these complications remain a significant clinical and financial burden worldwide. Their pathogenesis is influenced by genetic polymorphism and advanced glycation end products (AGEs). Chronic metabolic stress leads to the formation of AGEs via oxidative and nonenzymatic glycation. AGEs bind to the AGE receptor (RAGE) and actively cause microvascular damage. This occurs through endothelial dysfunction, amplification of oxidative stress, protein cross-linking, and inflammatory activation. Genes controlling AGE production, AGE-RAGE signaling, oxidative stress responses, endothelial nitric oxide bioavailability, and extracellular matrix remodeling affect individual susceptibility to AGE-mediated microvascular damage. Elevated AGE load and genetic polymorphisms influence metabolic memory, microvascular injury, and redox signaling. This review article outlines the molecular mechanisms involving AGEs, genetic polymorphisms, and microvascular complications. Understanding AGE biology and genetic risk analysis could support management of diabetic microvascular complications and foster personalized medicine and preventive approaches beyond traditional glucose-centric frameworks.
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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.