Evidence map›Paper›PMID 31134076›Full record

ReviewFrontiers in immunology2019

Regulation of Toll-Like Receptor (TLR) Signaling Pathway by Polyphenols in the Treatment of Age-Linked Neurodegenerative Diseases: Focus on TLR4 Signaling.

Shofiul Azam, Md Jakaria, In-Su Kim, Joonsoo Kim, Md Ezazul Haque, Dong-Kug Choi

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 5 pooled it
13.9field-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

120 citing papers in PubMed, 5 syntheses or guidelines pooled it, 222 citations in OpenAlex.

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  9. Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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60 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

6 authors at 1 institution in 1 country.

Shofiul AzamDepartment of Applied Life Science & Integrated Bioscience, Graduate School, Konkuk University, Chungju-si, South Korea.
Md JakariaDepartment of Applied Life Science & Integrated Bioscience, Graduate School, Konkuk University, Chungju-si, South Korea.
In-Su KimDepartment of Integrated Bioscience & Biotechnology, Research Institute of Inflammatory Disease (RID), College of Biomedical and Health Science, Konkuk University, Chungju-si, South Korea.
Joonsoo KimDepartment of Applied Life Science & Integrated Bioscience, Graduate School, Konkuk University, Chungju-si, South Korea.
Md Ezazul HaqueDepartment of Applied Life Science & Integrated Bioscience, Graduate School, Konkuk University, Chungju-si, South Korea.
Dong-Kug ChoiDepartment of Applied Life Science & Integrated Bioscience, Graduate School, Konkuk University, Chungju-si, South Korea.
Konkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal dysfunction initiates several intracellular signaling cascades to release different proinflammatory cytokines and chemokines, as well as various reactive oxygen species. In addition to neurons, microglia, and astrocytes are also affected by this signaling cascade. This release can either be helpful, neutral or detrimental for cell survival. Toll-like receptors (TLRs) activate and signal their downstream pathway to activate NF-κB and pro-IL-1β, both of which are responsible for neuroinflammation and linked to the pathogenesis of different age-related neurological conditions. However, herein, recent aspects of polyphenols in the treatment of neurodegenerative diseases are assessed, with a focus on TLR regulation by polyphenols. Different polyphenol classes, including flavonoids, phenolic acids, phenolic alcohols, stilbenes, and lignans can potentially target TLR signaling in a distinct pathway. Further, some polyphenols can suppress overexpression of inflammatory mediators through TLR4/NF-κB/STAT signaling intervention, while others can reduce neuronal apoptosis via modulating the TLR4/MyD88/NF-κB-pathway in microglia/macrophages. Indeed, neurodegeneration etiology is complex and yet to be completely understood, it may be that targeting TLRs could reveal a number of molecular and pharmacological aspects related to neurodegenerative diseases. Thus, activating TLR signaling modulation via natural resources could provide new therapeutic potentiality in the treatment of neurodegeneration.

Indexed as

AgingApoptosisAstrocytesCell SurvivalCytokinesHumansMacrophagesMyeloid Differentiation Factor 88Neurodegenerative DiseasesPolyphenolsSignal TransductionToll-Like Receptor 4CytokinesMYD88 protein, humanMyeloid Differentiation Factor 88PolyphenolsTLR4 protein, humanToll-Like Receptor 4inflammasomeMyD88neurodegenerative diseaseNF-κBpolyphenolsToll-like receptor

Identifiers

PMID31134076
PMCPMC6522942
OpenAlexW2944010700

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.