Evidence map›Paper›PMID 31922472›Full record

ReviewEuropean journal of rheumatology2020

The contribution of mesenchymal transitions to the pathogenesis of systemic sclerosis.

Irene Rosa, Eloisa Romano, Bianca Saveria Fioretto, Mirko Manetti

Open access · diamondAbstract readReview
In one paragraph

Review in European journal of rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025
    Review
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  19. Cd34+ Stromal Cells/Telocytes in Normal and Pathological Skin.International journal of molecular sciences · 2021
    Review
  20. Endothelial-to-mesenchymal transition in systemic sclerosis.Clinical and experimental immunology · 2021
    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

4 authors at 1 institution in 1 country.

Irene RosaDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.ORCID http://orcid.org/0000-0001-6352-0175
Eloisa RomanoDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.ORCID http://orcid.org/0000-0003-2744-8625
Bianca Saveria FiorettoDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.ORCID http://orcid.org/0000-0001-9275-7593
Mirko ManettiDepartment of Experimental and Clinical Medicine, University of Florence, Florence, Italy.ORCID http://orcid.org/0000-0003-3956-8480
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a multifaceted connective tissue disease characterized by widespread vasculopathy and autoimmune reactions that evolve into progressive interstitial, perivascular, and vessel wall fibrosis that affects the skin and multiple internal organs. Such an uncontrolled fibrotic process gradually disrupts the physiologic architecture of the affected tissues and frequently leads to significant organ dysfunction, thus representing a major cause of death in SSc patients. The main fibrosis orchestrators in SSc are represented by chronically activated myofibroblasts, a peculiar population of mesenchymal cells combining the extracellular matrix-synthesizing features of fibroblasts with cytoskeletal characteristics of contractile smooth muscle cells. Multiple lines of evidence support the notion that profibrotic myofibroblasts may derive not only from the activation of tissue resident fibroblasts but also from a variety of additional cell types, including pericytes, epithelial cells, vascular endothelial cells and preadipocytes/adipocytes. Here we overview an emerging picture that espouses that several cell transitional processes may be novel essential contributors to the pool of profibrotic myofibroblasts in SSc, potentially representing new suitable targets for therapeutic purposes. An in-depth dissection of the multiple origins of myofibroblasts and the underlying molecular mechanisms may be crucial in the process of deciphering the cellular bases of fibrosis persistence and refractoriness to the treatment and, therefore, may help in developing more effective and personalized therapeutic opportunities for SSc patients.

Identifiers

PMID31922472
PMCPMC7647682
OpenAlexW2999927892

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.