Evidence map›Paper›PMID 37814128›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

Targeting MyD88: Therapeutic mechanisms and potential applications of the specific inhibitor ST2825.

Meiqi Liu, Wenyan Kang, Zhizhong Hu, Chengkun Wang, Yang Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Tumor-intrinsic TLR4 signaling as a context-dependent rheostat in glioblastoma.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
  2. Review
  3. Bioactive Polysaccharides and Phlorotannins fromJournal of microbiology and biotechnology · 2025
    Article
  4. Article
  5. Review
  6. 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 at 1 institution in 1 country.

Meiqi LiuHengyang Medical School, Cancer Research Institute, University of South China, Chang Sheng Xi Avenue 28, Hengyang City, Hunan, 421001, People's Republic of China.
Wenyan KangHengyang Medical School, Cancer Research Institute, University of South China, Chang Sheng Xi Avenue 28, Hengyang City, Hunan, 421001, People's Republic of China.
Zhizhong HuHengyang Medical School, Cancer Research Institute, University of South China, Chang Sheng Xi Avenue 28, Hengyang City, Hunan, 421001, People's Republic of China.
Chengkun WangHengyang Medical School, Cancer Research Institute, University of South China, Chang Sheng Xi Avenue 28, Hengyang City, Hunan, 421001, People's Republic of China. charleswck@usc.edu.cn.
Yang ZhangHengyang Medical School, Cancer Research Institute, University of South China, Chang Sheng Xi Avenue 28, Hengyang City, Hunan, 421001, People's Republic of China. yangyang@usc.edu.cn.ORCID http://orcid.org/0000-0003-4973-2678
University of South China · CN

Funding

The Touth Program of National Natural Science Foundation of China No. 81500169
6 · The paper itself

Abstract

backgroundMyeloid differentiation factor-88 (MyD88) is a crucial adapter protein that coordinates the innate immune response and establishes an adaptive immune response. The interaction of the Toll/Interleukin-1 receptor (IL-1R) superfamily with MyD88 triggers the activation of various signalling pathways such as nuclear factor-κB (NF-κB) and activator protein-1 (AP-1), promoting the production of a variety of immune and inflammatory mediators and potentially driving the development of a variety of diseases.

objectiveThis article will explore the therapeutic potential and mechanism of the MyD88-specific inhibitor ST2825 and describe its use in the treatment of several diseases. We envision future research and clinical applications of ST2825 to provide new ideas for the development of anti-inflammatory drugs and disease-specific drugs to open new horizons for the prevention and treatment of related inflammatory diseases. MATERIALS AND

methodsThis review analysed relevant literature in PubMed and other databases. All relevant studies on MyD88 inhibitors and ST2825 that were published in the last 20 years were used as screening criteria. These studies looked at the development and improvement of MyD88 inhibitors and ST2825.

resultsRecent evidence using the small-molecule inhibitor of ST2825 has suggested that blocking MyD88 activity can be used to treat diseases such as neuroinflammation, inflammatory diseases such as acute liver/kidney injury, or autoimmune diseases such as systemic lupus erythematosus and can affect transplantation immunity. In addition, ST2825 has potential therapeutic value in B-cell lymphoma with the MyD88 L265P mutation.

conclusionTargeting MyD88 is a novel therapeutic strategy, and scientific research is presently focused on the development of MyD88 inhibitors. The peptidomimetic compound ST2825 is a widely studied small-molecule inhibitor of MyD88. Thus, ST2825 may be a potential therapeutic small-molecule agent for modulating host immune regulation in inflammatory diseases and inflammatory therapy.

Indexed as

Myeloid Differentiation Factor 88NF-kappa BAnti-Inflammatory AgentsHeterocyclic Compounds, 2-RingSignal TransductionSpiro CompoundsAnti-Inflammatory AgentsHeterocyclic Compounds, 2-RingMyeloid Differentiation Factor 88NF-kappa BSpiro CompoundsST2825Anti-inflammatoryImmunityMyD88 inhibitorST2825Targeted therapy

Identifiers

PMID37814128
OpenAlexW4387448685

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.