Evidence map›Paper›PMID 29971007›Full record

ReviewFrontiers in physiology2018

Biomarkers for Pulmonary Vascular Remodeling in Systemic Sclerosis: A Pathophysiological Approach.

Balazs Odler, Vasile Foris, Anna Gungl, Veronika Müller, Paul M Hassoun, Grazyna Kwapiszewska, Horst Olschewski, Gabor Kovacs

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Treatable Traits in Systemic Sclerosis.Clinical reviews in allergy & immunology · 2023
    Review
  6. Article
  7. Biomarkers in Systemic Sclerosis: An Overview.Current issues in molecular biology · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 4 institutions in 3 countries.

Balazs OdlerLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Vasile ForisLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Anna GunglLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Veronika MüllerDepartment of Pulmonology, Semmelweis University, Budapest, Hungary.
Paul M HassounDivision of Pulmonary & Critical Care Medicine, Johns Hopkins University, Baltimore, MD, United States.
Grazyna KwapiszewskaLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Horst OlschewskiLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Gabor KovacsLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Ludwig Boltzmann Institute for Lung Vascular Research · ATMedical University of Graz · ATJohns Hopkins University · USSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe complication of systemic sclerosis (SSc) associated with high morbidity and mortality. There are several biomarkers of SSc-PAH, reflecting endothelial physiology, inflammation, immune activation, extracellular matrix, metabolic changes, or cardiac involvement. Biomarkers associated with diagnosis, disease severity and progression have been identified, however, very few have been tested in a prospective setting. Some antinuclear antibodies such as nucleosome antibodies (NUC), anti-centromere antibodies (CENP-A/B) and anti-U3-ribonucleoprotein (anti-U3-RNP) are associated with PAH while anti-U1-ribonucleoprotein (anti-U1-RNP) is associated with a reduced PAH risk. Anti-endothelin receptor and angiotensin-1 receptor antibodies might be good markers of SSc-PAH and progression of pulmonary vasculopathy. Regarding the markers reflecting immune activation and inflammation, there are many inconsistent results. CXCL-4 was associated with SSc progression including PAH and lung fibrosis. Growth differentiation factor (GDF)-15 was associated with PAH and mortality but is not specific for SSc. Among the metabolites, kynurenine was identified as diagnostic marker for PAH, however, its pathologic role in the disease is unclear. Endostatin, an angiostatic factor, was associated with heart failure and poor prognosis. Established heart related markers, such as N-terminal fragment of A-type natriuretic peptide/brain natriuretic peptide (NT-proANP, NT-proBNP) or troponin I/T are elevated in SSc-PAH but are not specific for the right ventricle and may be increased to the same extent in left heart disease. Taken together, there is no universal specific biomarker for SSc-PAH, however, there is a pattern of markers that is strongly associated with a risk of vascular complications in SSc patients. Further comprehensive, multicenter and prospective studies are warranted to develop reliable algorithms for detection and prognosis of SSc-PAH.

Indexed as

autoimmunebiomarkerfibrosisPAHpulmonary hypertensionsystemic sclerosisvascular

Identifiers

PMID29971007
PMCPMC6018494
OpenAlexW2807908056

What OpenQuestion holds

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LicenceCC BY
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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.