Evidence map›Paper›PMID 33322749›Full record

ReviewBiomolecules2020

Transforming Growth Factor-β Signaling in Fibrotic Diseases and Cancer-Associated Fibroblasts.

Xueke Shi, Christian D Young, Hongmei Zhou, Xiaojing Wang

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

146 citing papers in PubMed, 212 citations in OpenAlex.

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  20. Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026
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86 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 at 3 institutions in 2 countries.

Xueke ShiState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, China.
Christian D YoungDepartment of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Hongmei ZhouState Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Oral Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, China.
Xiaojing WangDepartment of Pathology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
University of Colorado Anschutz Medical Campus · USSichuan University · CNVA Eastern Colorado Health Care System · US

Funding

Elucidating Mechanism of Immune Evasion in Head and Neck CancersR01DE027329 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WANG, JING HONG, WANG, XIAO-JING · 2018 to 2022
$2.8M
Mechanisms of Dual Inhibition of TGFbeta/PD-L1 in HNSCCR01DE028420 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI WANG, JING HONG, WANG, XIAO-JING · 2019 to 2023
$2.7M
Identifying oral cancer stem cell properties affected by the microenvironmentR01DE024371 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI JIMENO, ANTONIO, WANG, XIAO-JING · 2014 to 2017
$2.1M
Mechanisms of Breaking Indolence in Squamous Cell CarcinomaI01BX003232 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI WANG, XIAO-JING · 2017 to 2025
–
BLRD VA I01 BX003232National Nature Science Foundation of China 81772898NIDCR NIH HHS R01 DE024371NIDCR NIH HHS R01 DE027329NIDCR NIH HHS R01 DE028420The State Scholarship Fund of China Scholarship Council 201906240271
6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) signaling is essential in embryo development and maintaining normal homeostasis. Extensive evidence shows that TGF-β activation acts on several cell types, including epithelial cells, fibroblasts, and immune cells, to form a pro-fibrotic environment, ultimately leading to fibrotic diseases. TGF-β is stored in the matrix in a latent form; once activated, it promotes a fibroblast to myofibroblast transition and regulates extracellular matrix (ECM) formation and remodeling in fibrosis. TGF-β signaling can also promote cancer progression through its effects on the tumor microenvironment. In cancer, TGF-β contributes to the generation of cancer-associated fibroblasts (CAFs) that have different molecular and cellular properties from activated or fibrotic fibroblasts. CAFs promote tumor progression and chronic tumor fibrosis via TGF-β signaling. Fibrosis and CAF-mediated cancer progression share several common traits and are closely related. In this review, we consider how TGF-β promotes fibrosis and CAF-mediated cancer progression. We also discuss recent evidence suggesting TGF-β inhibition as a defense against fibrotic disorders or CAF-mediated cancer progression to highlight the potential implications of TGF-β-targeted therapies for fibrosis and cancer.

Indexed as

Signal TransductionAnimalsCancer-Associated FibroblastsDisease ProgressionFibrosisHumansMolecular Targeted TherapyTransforming Growth Factor betaTransforming Growth Factor betaanti-fibrosis/cancer therapycancercancer-associated fibroblastfibroblastsfibrotic diseasesTGF-β signaling

Identifiers

PMID33322749
PMCPMC7763058
OpenAlexW3111278897

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.