Evidence map›Paper›PMID 24752182›Full record

ReviewNature reviews. Rheumatology2014

Fibrosis--a lethal component of systemic sclerosis.

Yuen Yee Ho, David Lagares, Andrew M Tager, Mohit Kapoor

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 2 pooled it
17.9field-weighted citation impact, top 1% 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

167 citing papers in PubMed, 2 syntheses or guidelines pooled it, 298 citations in OpenAlex.

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  15. Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025
    Review
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107 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.

Yuen Yee HoShriners Hospital for Children, Division of Surgical Research, McGill University, 1529 Cedar Avenue, Montreal, QC H3G1A6, Canada.
David LagaresPulmonary and Critical Care Unit and Centre for Immunology and Inflammatory Diseases, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA.
Andrew M TagerPulmonary and Critical Care Unit and Centre for Immunology and Inflammatory Diseases, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA.
Mohit KapoorThe Toronto Western Research Institute, Division of Orthopaedics, Toronto Western Hospital, The University Health Network, 60 Leonard Avenue, Toronto, ON M5T 2S8, Canada.
Massachusetts General Hospital · USMcGill University · CAToronto Western Hospital · CA

Funding

Protective Role of the S1P-S1P1 Pathway in Pulmonary FibrosisR01HL108975 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI TAGER, ANDREW M · 2011 to 2015
$1.8M
The LPA Pathway in Lung Fibrosis: Novel Mediators and New Therapeutic TargetsR01HL095732 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI TAGER, ANDREW M · 2009 to 2010
$922k
CIHRNHLBI NIH HHS R01 HL095732NHLBI NIH HHS R01-HL095732NHLBI NIH HHS R01 HL108975NHLBI NIH HHS R01-HL108975
6 · The paper itself

Abstract

Fibrosis is a pathological process characterized by excessive accumulation of connective tissue components in an organ or tissue. Fibrosis is produced by deregulated wound healing in response to chronic tissue injury or chronic inflammation, the hallmarks of rheumatic diseases. Progressive fibrosis, which distorts tissue architecture and results in progressive loss of organ function, is now recognized to be one of the major causes of morbidity and mortality in individuals with one of the most lethal rheumatic disease, systemic sclerosis (SSc). In this Review, we discuss the pathological role of fibrosis in SSc. We discuss the involvement of endothelium and pericyte activation, aberrant immune responses, endoplasmic reticulum stress and chronic tissue injury in the initiation of fibrosis in SSc. We then discuss fibroblast activation and myofibroblast differentiation that occurs in response to these initiating processes and is responsible for excessive accumulation of extracellular matrix. Finally, we discuss the chemical and mechanical signals that drive fibroblast activation and myofibroblast differentiation, which could serve as targets for new therapies for fibrosis in SSc.

Indexed as

FibrosisAutoantibodiesCell DifferentiationEndoplasmic ReticulumEndotheliumFibroblastsHumansPericytesScleroderma, SystemicSkinStress, MechanicalTranscription FactorsAutoantibodiesTranscription Factors

Identifiers

PMID24752182
OpenAlexW1518950845

What OpenQuestion 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 OpenQuestion graph.