Evidence map›Paper›PMID 32307910›Full record

ReviewJournal of cellular and molecular medicine2020

Extracellular S100A4 as a key player in fibrotic diseases.

Zhenzhen Li, Yanan Li, Shuangqing Liu, Zhihai Qin

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. S100A4 Orchestrates Fibroblast Fate to Drive Fibrotic Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Cell fusion in osteoclastogenesis.Biochemical Society transactions · 2025
    Review
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  12. Review
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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 at 2 institutions in 1 country.

Zhenzhen LiMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.ORCID 0000-0002-7035-6657
Yanan LiSchool of Medicine, Ruijin Hospital, Shanghai Jiaotong University, Shanghai, China.
Shuangqing LiuKey Laboratory of Protein and Peptide Pharmaceuticals, CAS-University of Tokyo Joint Laboratory of Structural Virology and Immunology, Institute of Biophysics, Chinese Academy of Sciences, University of the Chinese Academy of Sciences, Beijing, China.
Zhihai QinMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Chinese Academy of Sciences · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is characterized by fibroblast activation, extracellular matrix (ECM) accumulation and infiltration of inflammatory cells that sometimes leads to irreversible organ dysfunction. Considerable evidence now indicates that inflammation plays a critical role in the initiation and progression of organ fibrosis. S100A4 protein, a ubiquitous member of the S100 family, has recently been discovered as a potential factor implicated in fibrotic diseases. S100A4 protein is released at inflammatory site and has a certain biological function to promote cell motility, invasion, ECM remodelling, autophagy and angiogenesis. In addition, extracellular S100A4 is also a potential causation of inflammatory processes and induces the release of cytokines and growth factors under different pathological conditions. Elevated S100A4 level in patients' serum closely correlates with disease activity in several fibrotic diseases and serves as a useful biomarker for diagnosis and monitoring disease progression. Analyses of knockout mouse models have identified a functional role of extracellular S100A4 protein in fibrotic diseases, suggesting that suppressing its expression, release or function might be a promising therapeutic strategy. This review will focus on the role of extracellular S100A4 as a key regulator of pro-inflammatory signalling pathways and its relative biological processes involved in the pathogenesis of fibrosis.

Indexed as

DiseaseAnimalsExtracellular SpaceFibrosisHumansModels, BiologicalMolecular Targeted TherapyS100 Calcium-Binding Protein A4S100 Calcium-Binding Protein A4biomarkerdamage-associated molecular patternextracellular S100A4Fibrosisinflammation

Identifiers

PMID32307910
PMCPMC7294136
OpenAlexW3016647148

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.