Evidence map›Paper›PMID 40077627›Full record

ReviewNutrients2025

The Potential Role of Advanced Glycation End Products in the Development of Kidney Disease.

Yibin Ma, Xinyu Wang, Shan Lin, Lei King, Liegang Liu

Abstract readReview
In one paragraph

Review in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
  2. Article
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  4. Review
  5. Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Metabolic Crosstalk in Diabetic Kidney Disease: Synergistic Effects of Glucotoxicity and Lipotoxicity.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
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  17. Review
  18. Article
  19. Article
  20. Review
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.

Yibin MaDepartment of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Xinyu WangDepartment of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Shan LinDepartment of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Lei KingDepartment of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.ORCID 0000-0001-6765-7080
Liegang LiuDepartment of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.ORCID 0000-0002-7029-1224

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced glycation end products (AGEs) represent a class of toxic and irreversible compounds formed through non-enzymatic reactions between proteins or lipids and carbonyl compounds. AGEs can arise endogenously under normal metabolic conditions and in pathological states such as diabetes, kidney disease, and inflammatory disorders. Additionally, they can be obtained exogenously through dietary intake, particularly from foods high in fat or sugar, as well as grilled and processed items. AGEs accumulate in various organs and have been increasingly recognized as significant contributors to the progression of numerous diseases, particularly kidney disease. As the kidney plays a crucial role in AGE metabolism and excretion, it is highly susceptible to AGE-induced damage. In this review, we provide a comprehensive discussion on the role of AGEs in the onset and progression of various kidney diseases, including diabetic nephropathy, chronic kidney disease, and acute kidney injury. We explore the potential biological mechanisms involved, such as AGE accumulation, the AGEs-RAGE axis, oxidative stress, inflammation, gut microbiota dysbiosis, and AGE-induced DNA damage. Furthermore, we discuss recent findings on the metabolic characteristics of AGEs in vivo and their pathogenic impact on renal function. Additionally, we examine the clinical significance of AGEs in the early diagnosis, treatment, and prognosis of kidney diseases, highlighting their potential as biomarkers and therapeutic targets. By integrating recent advancements in AGE research, this review aims to provide new insights and strategies for mitigating AGE-related renal damage and improving kidney disease management.

Indexed as

Glycation End Products, AdvancedKidney DiseasesAnimalsBiomarkersDiabetic NephropathiesDNA DamageGastrointestinal MicrobiomeHumansKidneyOxidative StressRenal Insufficiency, ChronicBiomarkersGlycation End Products, Advancedadvanced glycation end products (AGEs)kidney diseasekidney function

Identifiers

PMID40077627
PMCPMC11902189

What OpenQuestion holds

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Registered trials

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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.