Evidence map›Paper›PMID 42053959›Full record

ReviewInflammopharmacology2026

Pharmaco-therapeutic modulation of the Glo1-Nrf2-RAGE functional network in chronic inflammation: polyphenols in the context of current anti-inflammatory therapy.

Sajid Ali, Muhammad Saeed Akhtar, Adnan Amin, Atif Ali Khan Khalil, Wajid Zaman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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.

Sajid AliDepartment of Horticulture and Life Science, Yeungnam University, Gyeongsan, 38541, Republic of Korea.
Muhammad Saeed AkhtarDepartment of Chemistry, Yeungnam University, Gyeongsan, 38541, Republic of Korea. msakhtar@yu.ac.kr.
Adnan Amin3Department of Life Sciences, Yeungnam University, Gyeongsan, 38541, Republic of Korea.
Atif Ali Khan KhalilDepartment of Biotechnology, Yeungnam University, Gyeongsan, 38541, Republic of Korea.
Wajid Zaman3Department of Life Sciences, Yeungnam University, Gyeongsan, 38541, Republic of Korea. wajidzaman@yu.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation is a central driver of numerous disorders, including metabolic, cardiovascular, neurodegenerative, autoimmune, and malignant diseases. Although current anti-inflammatory pharmaco-therapeutic strategies, including nonsteroidal anti-inflammatory drugs, corticosteroids, immunosuppressants, disease-modifying antirheumatic drugs, and biologic agents, can reduce inflammatory burden and improve clinical outcomes, their long-term use is often limited by adverse effects, incomplete disease control, treatment resistance, and poor correction of upstream oxidative and glycation-related mechanisms. In this context, the interconnected Glo1-Nrf2-RAGE network has emerged as a pharmacologically relevant framework that links carbonyl stress, oxidative injury, and inflammatory signal amplification in chronic diseases. This review examines the therapeutic significance of this axis and evaluates polyphenolic compounds as emerging modulators of Glo1-, Nrf2-, and RAGE-associated pathways. Polyphenols such as curcumin, epigallocatechin gallate, resveratrol, and related phenolics exhibit anti-inflammatory effects in preclinical models by enhancing antioxidant defense, attenuating AGE-RAGE signaling, and reducing pro-inflammatory mediators. However, their clinical translation remains constrained by poor bioavailability, variable pharmacokinetics, lack of dose standardization, and limited human evidence. Positioning polyphenols within the broader landscape of anti-inflammatory therapy helps clarify their current value as adjunctive modulators or lead structures for future therapeutic development targeting chronic inflammation.

Indexed as

Anti-Inflammatory AgentsInflammationNF-E2-Related Factor 2PolyphenolsReceptor for Advanced Glycation End ProductsAnimalsChronic DiseaseHumansOxidative StressSignal TransductionAnti-Inflammatory AgentsNFE2L2 protein, humanNF-E2-Related Factor 2PolyphenolsReceptor for Advanced Glycation End ProductsAnti-inflammatory therapyChronic inflammationGlo1–Nrf2–RAGE axisOxidative stressPharmacological modulationPolyphenolic compounds

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.