Evidence map›Paper›PMID 39943886›Full record

ReviewCurrent opinion in rheumatology2025

An update on the pathogenesis of idiopathic inflammatory myopathies.

Eleni Tiniakou

Abstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

1 author.

Eleni TiniakouDivision of Rheumatology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.

Funding

RNA: Polymerase III specific CD8+ T cells: a mechanistic insight into cancer-induced autoimmunity in sclerodermaK08AR077732 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TINIAKOU, ELENI · 2021 to 2025
$794k
NIAMS NIH HHS K08 AR077732
6 · The paper itself

Abstract

purpose of reviewAs the question of the pathogenesis of inflammatory myopathies remains unanswered, there has been a significant effort in recent years to investigate various components of the innate and adaptive immune systems, with evidence pointing that they work together to initiate and propagate the autoimmune response. This review aims to explore recent advancements in understanding the mechanisms underlying myopathies. RECENT

findingsRecent research has concentrated on uncovering potential triggers, examining the role of immune cells, both lymphocytes and myeloids, and investigating the contribution of inflammatory mediators to the autoimmune response in inflammatory myopathies. Unsuccessful clinical trials helped reshape established hypotheses about pathogenesis, while genetic mutations offered clues to the disease's root causes. The pathogenic role of autoantibodies is being reconsidered based on transcriptional data. Repurposing existing medications to combat muscle fiber dysfunction is also emerging as a potential therapeutic approach. SUMMARY: Our understanding of inflammatory myopathies has evolved significantly as our understanding of the disease has grown. Even though breakthroughs have been documented on the underlying mechanisms of myopathies, important questions remain unanswered.

Indexed as

MyositisAutoantibodiesHumansAutoantibodies

Identifiers

PMID39943886
PMCPMC12452227

What OpenQuestion holds

Textmetadata
LicenceTDM
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.