Evidence map›Paper›PMID 40423634›Full record

ReviewAging and disease2025

Type 2 Diabetes Mellitus: A Metabolic Model of Accelerated Aging - Multi-Organ Mechanisms and Intervention Approaches.

Ziran Zhang, Xiaolin He, Yuxin Sun, Jitong Li, Jia Sun

Abstract readReview
In one paragraph

Review in Aging and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

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  9. Frontiers in pharmacology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Ziran Zhang
Xiaolin He
Yuxin Sun
Jitong Li
Jia Sun

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by chronic high blood sugar levels and insulin resistance (IR). Modern medicine has shown that diabetes plays a role in speeding up the aging process of the body independently of age, making it an age-related aging disease. The oxidative stress caused by chronic high blood sugar and IR can lead to dysfunctional mitochondria, which in turn promotes changes in epigenetic regulation, shortening of telomeres, and cellular senescence. There is currently a lot of interest in understanding how T2DM contributes to senescence. This review synthesizes epidemiological and clinical research findings on aging across various organs, focusing on insulin resistance and oxidative stress as primary mechanisms. It introduces four diabetes-specific aging axes: glucose toxicity, toxicity of advanced glycation end-products (AGEs), immunoinflammatory aging, and protein amyloidosis, which are integrated into the "metabolism-inflammation-aging" network. Additionally, we provide new insights into interventions targeting aging in diabetes.

Indexed as

AgingDiabetes Mellitus, Type 2AnimalsGlycation End Products, AdvancedHumansInsulin ResistanceOxidative StressGlycation End Products, Advanced

Identifiers

PMID40423634
PMCPMC13061546

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.