Evidence map›Paper›PMID 26317679›Full record

ReviewCurrent opinion in rheumatology2015

Genetics of systemic sclerosis: recent advances.

Paula S Ramos, Richard M Silver, Carol A Feghali-Bostwick

Open access · hybridAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  12. Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

3 authors at 2 institutions in 1 country.

Paula S RamosaDivision of Rheumatology and Immunology, Department of Medicine bDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, South Carolina, USA.
Richard M Silver
Carol A Feghali-Bostwick
Center for Rheumatology · USMedical University of South Carolina · US

Funding

SOUTH CAROLINA CLINICAL & TRANSLATIONAL RESEARCH INSTITUTE (SCTR)UL1RR029882 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$10.1M
South Carolina Clinical & Translational Research Institute (SCTR)UL1TR000062 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2012 to 2014
$9.4M
Patient Resource CoreP60AR062755 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI GILKESON, GARY S · 2012 to 2016
$5.8M
Rheumatic Diseases Research Core CentersP30AR061271 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WHITFIELD, MICHAEL L · 2011 to 2015
$3.1M
Scleroderma Twin Study and analysis of Estrogen in patients with dcSScK24AR060297 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FEGHALI-BOSTWICK, CAROL A. · 2013 to 2025
$1.4M
The role of natural selection in SLE risk among African-AmericansK01AR067280 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAMOS, PAULA SOFIA · 2015 to 2018
$516k
Safety & Suitability of Dabigatran to Inhibit Thrombin in SclerodermaR21AR065089 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SILVER, RICHARD M. · 2015 to 2016
$327k
DNA methylation biomarkers of scleroderma-associated interstitial lung diseaseR03AR065801 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAMOS, PAULA SOFIA · 2014 to 2016
$231k
NCATS NIH HHS UL1 TR000062NCRR NIH HHS UL1 RR029882NIAMS NIH HHS K01 AR067280NIAMS NIH HHS K24 AR060297NIAMS NIH HHS P30 AR061271NIAMS NIH HHS P60 AR062755NIAMS NIH HHS R03 AR065801NIAMS NIH HHS R21 AR065089
6 · The paper itself

Abstract

purpose of reviewLarge-scale and follow-up genetic association studies in systemic sclerosis (SSc) have implicated over 40 regions in disease risk, 15 of which with robust associations. Nevertheless, the causal variants and the functional mechanisms underlying the genetic associations remain elusive, and the reasons for the higher disease burden in African Americans unknown. Incorporating tools from diverse fields is beginning to unveil the role of genetic diversity and regulatory variation in SSc susceptibility. This review will summarize recent advances in SSc genetics, including autoimmune disease overlap, evidence of natural selection, and current progress towards the dissection of the functional role of associated risk variants. RECENT

findingsIn the past year, multiple large-scale studies reported novel strong and suggestive SSc associations. These results, coupled with the regions shared with other autoimmune diseases, emphasize the role of dysregulation of immune pathways as a key causative factor in SSc pathogenesis. Strong evidence implicates natural selection as a mechanism contributing to the maintenance of some of these SSc alleles in the population. Studies integrating genomic, transcriptomic, and epigenomic datasets in specific cell types to identify causal autoimmune disease variants are emerging. SUMMARY: The identification and comprehensive understanding of the factors and mechanisms contributing to SSc will contribute to improved diagnosis and disease management.

Indexed as

HumansScleroderma, Systemic

Identifiers

PMID26317679
PMCPMC4608482
OpenAlexW1223222859

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.