Evidence map›Paper›PMID 32268503›Full record

ReviewInternational journal of molecular sciences2020

The Vascular Involvement in Soft Tissue Fibrosis-Lessons Learned from Pathological Scarring.

Chenyu Huang, Rei Ogawa

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
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  4. Chronic radiation-induced dermatitis: what is new in 2024? A narrative review.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2026
    Review
  5. Review
  6. The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
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  8. Article
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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

2 authors at 2 institutions in 2 countries.

Chenyu HuangDepartment of Dermatology, School of Clinical Medicine, Tsinghua University, Beijing 100084, China.ORCID 0000-0001-9521-5650
Rei OgawaDepartment of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, Tokyo 113-8603, Japan.ORCID 0000-0003-3658-555X
Nippon Medical School · JPTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Soft tissue fibrosis in important organs such as the heart, liver, lung, and kidney is a serious pathological process that is characterized by excessive connective tissue deposition. It is the result of chronic but progressive accumulation of fibroblasts and their production of extracellular matrix components such as collagens. Research on pathological scars, namely, hypertrophic scars and keloids, may provide important clues about the mechanisms that drive soft tissue fibrosis, in particular the vascular involvement. This is because these dermal fibrotic lesions bear all of the fibrotic characteristics seen in soft tissue fibrosis. Moreover, their location on the skin surface means they are readily observable and directly treatable and therefore more accessible to research. We will focus here on the roles that blood vessel-associated cells play in cutaneous scar pathology and assess from the literature whether these cells also contribute to other soft tissue fibroses. These cells include endothelial cells, which not only exhibit aberrant functions but also differentiate into mesenchymal cells in pathological scars. They also include pericytes, hepatic stellate cells, fibrocytes, and myofibroblasts. This article will review with broad strokes the roles that these cells play in the pathophysiology of different soft tissue fibroses. We hope that this brief but wide-ranging overview of the vascular involvement in fibrosis pathophysiology will aid research into the mechanisms underlying fibrosis and that this will eventually lead to the development of interventions that can prevent, reduce, or even reverse fibrosis formation and/or progression.

Indexed as

Neovascularization, PathologicAnimalsCell CommunicationCicatrixConnective TissueEndothelial CellsEndotheliumFibroblastsFibrosisHepatic Stellate CellsHumansMyofibroblastsOrgan SpecificityPericytesendothelial dysfunctionendothelial-to-mesenchymal cell transitionfibrocyteshepatic stellate cellsmyofibroblastspathological scarspericytessoft tissue fibrosisvascular involvement

Identifiers

PMID32268503
PMCPMC7177855
OpenAlexW3014703025

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.