Evidence map›Paper›PMID 38230363›Full record

ArticleCurrent treatment options in rheumatology2023

Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.

Alexander Ghincea, Samuel Woo, Sheeline Yu, Taylor Pivarnik, Vitoria Fiorini, Erica L Herzog, Changwan Ryu

Open access · hybridAbstract read
In one paragraph

Article in Current treatment options in rheumatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

7 authors at 1 institution in 1 country.

Alexander GhinceaYale School of Medicine, Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine.
Samuel WooYale School of Medicine, Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine.
Sheeline YuYale School of Medicine, Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine.
Taylor PivarnikYale School of Medicine, Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine.
Vitoria FioriniYale School of Medicine, Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine.
Erica L HerzogYale School of Medicine, Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine.
Changwan RyuYale School of Medicine, Department of Internal Medicine, Section of Pulmonary, Critical Care, and Sleep Medicine.
Yale University · US

Funding

Training Translational Lung Biology and PathobiologyT32HL007778 · NHLBI · YALE UNIVERSITY · PI Erica L Herzog, NAFTALI KAMINSKI · 1994 to 2026
$14.4M
Macrophage driven, profibrotic adrenergic nerve remodeling in SSc-ILDR01HL152677 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2020 to 2023
$2.4M
Neuroimmune Molecules in Scleroderma Lung FibrosisR01HL125850 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2016 to 2019
$1.7M
Mitochondrial DNA and TLR9 in Pulmonary FibrosisK08HL151970 · NHLBI · YALE UNIVERSITY · PI RYU, CHANGWAN · 2020 to 2024
$840k
NHLBI NIH HHS K08 HL151970NHLBI NIH HHS R01 HL125850NHLBI NIH HHS R01 HL152677NHLBI NIH HHS T32 HL007778
6 · The paper itself

Abstract

Purpose of the review: Systemic sclerosis (SSc) is a condition of dermal and visceral scar formation characterized by immune dysregulation and inflammatory fibrosis. Approximately 90% of SSc patients develop interstitial lung disease (ILD), and it is the leading cause of morbidity and mortality. Further understanding of immune-mediated fibroproliferative mechanisms has the potential to catalyze novel treatment approaches in this difficult to treat disease. Recent findings: Recent advances have demonstrated the critical role of aberrant innate immune activation mediated by mitochondrial DNA (mtDNA) through interactions with toll-like receptor 9 (TLR9) and cytosolic cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS). Summary: In this review, we will discuss how the nature of the mtDNA, whether oxidized or mutated, and its mechanism of release, either intracellularly or extracellularly, can amplify fibrogenesis by activating TLR9 and cGAS, and the novel insights gained by interrogating these signaling pathways. Because the scope of this review is intended to generate hypotheses for future research, we conclude our discussion with several important unanswered questions.

Indexed as

cGAS-STINGInterstitial lung diseasemitochondial DNASystemic SclerosisTLR9

Identifiers

PMID38230363
PMCPMC10791121
OpenAlexW4385663380

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.