Evidence map›Paper›PMID 27886187›Full record

Trial reportScientific reports2016

Plasma Proteomic Study in Pulmonary Arterial Hypertension Associated with Congenital Heart Diseases.

Xi Zhang, Hai-Tao Hou, Jun Wang, Xiao-Cheng Liu, Qin Yang, Guo-Wei He

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Proteomic analysis of pulmonary arterial hypertension.Therapeutic advances in chronic disease · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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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

6 authors at 3 institutions in 2 countries.

Xi ZhangDepartment of Surgery &Center for Basic Medical Research, TEDA International Cardiovascular Hospital, Chinese Academy of Medical Sciences (CAMS) &Peking Union Medical College (PUMC), Tianjin &The Affiliated Hospital of Hangzhou Normal University &Zhejiang University, Hangzhou, China.
Hai-Tao HouTEDA International Cardiovascular Hospital, CAMS &PUMC, Tianjin, China.
Jun WangTEDA International Cardiovascular Hospital, CAMS &PUMC, Tianjin, China.
Xiao-Cheng LiuTEDA International Cardiovascular Hospital, CAMS &PUMC, Tianjin, China.
Qin YangTEDA International Cardiovascular Hospital, CAMS &PUMC, Tianjin, China.
Guo-Wei HeDepartment of Surgery &Center for Basic Medical Research, TEDA International Cardiovascular Hospital, Chinese Academy of Medical Sciences (CAMS) &Peking Union Medical College (PUMC), Tianjin &The Affiliated Hospital of Hangzhou Normal University &Zhejiang University, Hangzhou, China.
TEDA International Cardiovascular Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNOregon Health & Science University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension associated with congenital heart disease (CHD-PAH) has serious consequence and plasma protein profiles in CHD-PAH are unknown. We aimed to reveal the differential plasma proteins in 272 CHD patients with or without PAH. Various types of CHD-PAH were studied. Differential plasma proteins were first detected by iTRAQ proteomic technology and those with significant clinical relevance were selected for further ELISA validation in new cohort of patients. Among the 190 differential plasma proteins detected by iTRAQ, carbamoyl-phosphate synthetase I (CPSI, related to urea cycle and endogenous nitric oxide production) and complement factor H-related protein 2 (CFHR2, related to complement system and coagulant mechanism) were selected for further ELISA validation in new cohort of 152 patients. Both CPSI and CFHR2 were down-regulated with decreased plasma levels (p < 0.01). Thus, we for the first time in CHD-PAH patients identified a large number of differential plasma proteins. The decreased CPSI expression in CHD-PAH patients may reveal a mechanism related to endogenous nitric oxide and the decrease of CFHR2 protein may demonstrate the deficiency of the immune system and coagulation mechanism. The findings may open a new direction for translational medicine in CHD-PAH with regard to the diagnosis and progress of the disease.

Indexed as

ProteomicsBlood ProteinsChildChild, PreschoolFemaleHeart Defects, CongenitalHumansHypertension, PulmonaryMaleBlood Proteins

Identifiers

PMID27886187
PMCPMC5122864
OpenAlexW2554647114

What OpenQuestion holds

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LicenceCC BY
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.