Evidence map›Paper›PMID 42074100›Full record

ReviewInternational journal of molecular sciences2026

CC Chemokines in Myocardial Fibrosis: Regulatory Networks of CCL17 and Emerging Therapeutic Implications.

Weiting Cai, Jing Zhao, Zheng Zhang

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Weiting CaiDepartment of Coronary Care Unit, The First Hospital of Lanzhou University, Lanzhou 730000, China.ORCID 0009-0008-7843-1480
Jing ZhaoHeart Center, The First Hospital of Lanzhou University, Lanzhou 730000, China.
Zheng ZhangHeart Center, The First Hospital of Lanzhou University, Lanzhou 730000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial fibrosis is a key pathological process driving the progression of cardiovascular diseases toward heart failure, closely linked to persistent inflammation and immune dysregulation. Among CC chemokines, CCL17 has emerged as an important mediator connecting immune cell dynamics with fibrotic remodeling. This review outlines current understanding of the cellular sources, regulatory mechanisms, and functional roles of CCL17, with particular attention to its impact on regulatory T cell (Treg) recruitment through ligand-biased signaling. Beyond this mechanism, CCL17 likely operates within a broader inflammatory network, with potential interactions involving CCR2

Indexed as

CardiomyopathiesChemokine CCL17Chemokines, CCMyocardiumAnimalsFibrosisHumansSignal TransductionT-Lymphocytes, RegulatoryChemokine CCL17Chemokines, CCcardiac remodelingCC chemokinesCCL17heart failuremyocardial fibrosisregulatory T cells

Identifiers

PMID42074100
PMCPMC13115924

What Socratic 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 Socratic graph.