Evidence map›Paper›PMID 40102851›Full record

ReviewCell communication and signaling : CCS2025

An examination of the LPS-TLR4 immune response through the analysis of molecular structures and protein-protein interactions.

Ruiqin Luo, Yuexin Yao, Zhuo Chen, Xiaoming Sun

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing 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

104 citing papers in PubMed.

  1. Review
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  4. Modulation of the gut microbiota by traditional Chinese medicine to attenuate chemotherapy-induced toxicity in gastric cancer: a review.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
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44 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

4 authors.

Ruiqin Luo *School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, 442000, China.
Yuexin Yao *School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, 442000, China.
Zhuo ChenSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan, 442000, China. chenzhuo@whu.edu.cn.
Xiaoming SunSchool of Basic Medical Sciences, Hubei University of Medicine, Shiyan, 442000, China. 151321820@163.com.

Funding

National Natural Science Foundation of China No. 82104205National Natural Science Foundation of China No. 82472302Natural Science Foundation of Hubei Province No. 2023AFB853Natural Science Foundation of Hubei Province No. 2024AFB802
6 · The paper itself

Abstract

The LPS-TLR4 immune response is a critical mechanism in the body's defense against Gram-negative bacterial infections, yet its dysregulation can lead to severe inflammatory diseases. Lipopolysaccharide (LPS), a pivotal pathogen-associated molecular pattern (PAMP) on the surface of gram-negative bacteria, is recognized by Toll-like receptor 4 (TLR4), initiating a complex cascade of immune responses. This review delves into the intricate molecular structures and protein-protein interactions that underpin the LPS-TLR4 signaling pathway, offering a comprehensive analysis of both extracellular recognition and intracellular signal transduction. We explore the roles of key molecules such as LBP, CD14, MD-2, and TLR4 in the initial recognition of LPS, followed by the downstream signaling pathways mediated by MyD88-dependent and MyD88-independent mechanisms. The MyD88-dependent pathway primarily activates NF-κB and AP-1, leading to macrophage M1 polarization and the release of pro-inflammatory cytokines, while the MyD88-independent pathway triggers IRF activation and type-I interferon production. By elucidating the structural basis and functional interactions of these signaling molecules, this review not only enhances our understanding of the LPS-TLR4 immune response but also highlights its implications in both infectious and non-infectious diseases. Our findings underscore the potential of targeting this pathway for therapeutic interventions, offering new avenues for the treatment of inflammatory and immune-related disorders.

Indexed as

LipopolysaccharidesToll-Like Receptor 4AnimalsHumansMyeloid Differentiation Factor 88Protein BindingSignal TransductionLipopolysaccharidesMyeloid Differentiation Factor 88Toll-Like Receptor 4Immune responseLPSMolecular structurePattern recognition receptorTLR4 Signal transduction

Identifiers

PMID40102851
PMCPMC11921546

What OpenQuestion holds

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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.