Evidence map›Paper›PMID 29674613›Full record

ReviewNature reviews. Rheumatology2018

Risk factors and disease mechanisms in myositis.

Frederick W Miller, Janine A Lamb, Jens Schmidt, Kanneboyina Nagaraju

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00017914 (Studies in the Natural History and Pathogenesis of Childhood-Onset and Adult-Onset Idiopathic Inflammatory Myopathies), which is not on this map. Cited by 95 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 2 pooled it
11.2field-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.

NCT00017914 recruitingnot on this map

Studies in the Natural History and Pathogenesis of Childhood-Onset and Adult-Onset Idiopathic Inflammatory Myopathies

TypeobservationalSponsorNational Institute of Environmental Health Sciences (NIEHS)Ran1995Enrolled1,200ConditionsDermatomyositis, Polymyositis, Inclusion Body Myositis
3 · Its place in the literature

Who cites it

95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 193 citations in OpenAlex.

  1. Pooled it
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  19. A window into intracellular events in myositis through subcellular proteomics.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  20. Cardiac Involvement in Idiopathic Inflammatory Myopathies.Journal of inflammation research · 2025
    Review

35 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 4 institutions in 3 countries.

Frederick W MillerEnvironmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Janine A LambCentre for Epidemiology, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, UK.
Jens SchmidtDepartment of Neurology, University Medical Center Göttingen, Göttingen, Germany.
Kanneboyina NagarajuDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, Binghamton University, Binghamton, NY, USA.
Binghamton University · USManchester Academic Health Science Centre · GBNational Institute of Environmental Health Sciences · USUniversitätsmedizin Göttingen · DE

Funding

Environmental/genetic Risk Factors and Pathogenesis of Autoimmune DiseaseZIAES101074 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RIDER, LISA · 2009 to 2025
$34.6M
Virus induced genetic changes in the pathogenesis of autoimmune myositisR21AI128248 · NIAID · STATE UNIVERSITY OF NY,BINGHAMTON · PI NAGARAJU, KANNEBOYINA · 2017 to 2018
$437k
Preclinical drug trial in mouse models of inflammationK26OD011171 · OD · STATE UNIVERSITY OF NY,BINGHAMTON · PI NAGARAJU, KANNEBOYINA · 2012 to 2015
$420k
Intramural NIH HHS Z99 ES999999Medical Research Council MR/N003322/1NIAID NIH HHS R21 AI128248NIH HHS K26 OD011171
6 · The paper itself

Abstract

Autoimmune diseases develop as a result of chronic inflammation owing to interactions between genes and the environment. However, the mechanisms by which autoimmune diseases evolve remain poorly understood. Newly discovered risk factors and pathogenic processes in the various idiopathic inflammatory myopathy (IIM) phenotypes (known collectively as myositis) have illuminated innovative approaches for understanding these diseases. The HLA 8.1 ancestral haplotype is a key risk factor for major IIM phenotypes in some populations, and several genetic variants associated with other autoimmune diseases have been identified as IIM risk factors. Environmental risk factors are less well studied than genetic factors but might include viruses, bacteria, ultraviolet radiation, smoking, occupational and perinatal exposures and a growing list of drugs (including biologic agents) and dietary supplements. Disease mechanisms vary by phenotype, with evidence of shared innate and adaptive immune and metabolic pathways in some phenotypes but unique pathways in others. The heterogeneity and rarity of the IIMs make advancements in diagnosis and treatment cumbersome. Novel approaches, better-defined phenotypes, and international, multidisciplinary consensus have contributed to progress, and it is hoped that these methods will eventually enable therapeutic intervention before the onset or major progression of disease. In the future, preemptive strategies for IIM management might be possible.

Indexed as

Disease ManagementEnvironmental ExposureGenetic HeterogeneityGenetic Predisposition to DiseaseHaplotypesHLA AntigensHumansMyositisPhenotypeHLA Antigens

Identifiers

PMID29674613
PMCPMC6745704
OpenAlexW2792190570

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.