Evidence map›Paper›PMID 33261212›Full record

ReviewMolecules (Basel, Switzerland)2020

The Development of Maillard Reaction, and Advanced Glycation End Product (AGE)-Receptor for AGE (RAGE) Signaling Inhibitors as Novel Therapeutic Strategies for Patients with AGE-Related Diseases.

Chieh-Yu Shen, Cheng-Hsun Lu, Cheng-Han Wu, Ko-Jen Li, Yu-Min Kuo, Song-Chou Hsieh, Chia-Li Yu

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 4 pooled it
16.0field-weighted citation impact, top 1% of its field
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

136 citing papers in PubMed, 4 syntheses or guidelines pooled it, 270 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. The Role of Glycolysis in Diabetic Kidney Disease.International journal of molecular sciences · 2026
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  14. Quercetin alleviates CClBiochemistry and biophysics reports · 2026
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76 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 1 country.

Chieh-Yu ShenInstitute of Clinical Medicine, National Taiwan University College of Medicine, Taipei 10002, Taiwan.
Cheng-Hsun LuInstitute of Clinical Medicine, National Taiwan University College of Medicine, Taipei 10002, Taiwan.
Cheng-Han WuInstitute of Clinical Medicine, National Taiwan University College of Medicine, Taipei 10002, Taiwan.
Ko-Jen LiDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei 10002, Taiwan.ORCID 0000-0002-4544-4620
Yu-Min KuoInstitute of Clinical Medicine, National Taiwan University College of Medicine, Taipei 10002, Taiwan.
Song-Chou HsiehDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei 10002, Taiwan.
Chia-Li YuDepartment of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei 10002, Taiwan.
National Taiwan University · TWNational Taiwan University Hospital · TWKaohsiung Medical University · TW

Funding

Academia Sinica AS-KPQ-109-BioMedAcademia Sinica AS-SUMMIT-109Ministry of Science and Technology, Taiwan MOST 109-0210-01-18-02National Taiwan University Hospital 109-07National Taiwan University Hospital 109-M4565
6 · The paper itself

Abstract

Advanced glycation end products (AGEs) are generated by nonenzymatic modifications of macromolecules (proteins, lipids, and nucleic acids) by saccharides (glucose, fructose, and pentose) via Maillard reaction. The formed AGE molecules can be catabolized and cleared by glyoxalase I and II in renal proximal tubular cells. AGE-related diseases include physiological aging, neurodegenerative/neuroinflammatory diseases, diabetes mellitus (DM) and its complications, autoimmune/rheumatic inflammatory diseases, bone-degenerative diseases, and chronic renal diseases. AGEs, by binding to receptors for AGE (RAGEs), alter innate and adaptive immune responses to induce inflammation and immunosuppression via the generation of proinflammatory cytokines, reactive oxygen species (ROS), and reactive nitrogen intermediates (RNI). These pathological molecules cause vascular endothelial/smooth muscular/connective tissue-cell and renal mesangial/endothelial/podocytic-cell damage in AGE-related diseases. In the present review, we first focus on the cellular and molecular bases of AGE-RAGE axis signaling pathways in AGE-related diseases. Then, we discuss in detail the modes of action of newly discovered novel biomolecules and phytochemical compounds, such as Maillard reaction and AGE-RAGE signaling inhibitors. These molecules are expected to become the new therapeutic strategies for patients with AGE-related diseases in addition to the traditional hypoglycemic and anti-hypertensive agents. We particularly emphasize the importance of "metabolic memory", the "French paradox", and the pharmacokinetics and therapeutic dosing of the effective natural compounds associated with pharmacogenetics in the treatment of AGE-related diseases. Lastly, we propose prospective investigations for solving the enigmas in AGE-mediated pathological effects.

Indexed as

Maillard ReactionAnimalsDiabetes MellitusGlycation End Products, AdvancedHumansInflammationNeurodegenerative DiseasesPhytochemicalsReceptor for Advanced Glycation End ProductsSignal TransductionGlycation End Products, AdvancedPhytochemicalsReceptor for Advanced Glycation End Productsadvanced glycation end productsAGE–RAGE axis signalingAGE-related diseasesglyoxalaseMaillard reactionMaillard reaction inhibitormetabolic memoryNε(carboxyethyl)-lysineNε-(carboxymethyl)-lysinereceptor for AGEs

Identifiers

PMID33261212
PMCPMC7729569
OpenAlexW3106899554

What OpenQuestion holds

Textmetadata
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.