Evidence map›Paper›PMID 39513871›Full record

ArticleCells2024

Comparative Analysis of Plasma Protein Dynamics in Women with ST-Elevation Myocardial Infarction and Takotsubo Syndrome.

Shafaat Hussain, Sandeep Jha, Evelin Berger, Linnea Molander, Valentyna Sevastianova, Zahra Sheybani, Aaron Shekka Espinosa, Ahmed Elmahdy, Amin Al-Awar, Yalda Kakaei and 9 more

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

19 authors.

Shafaat HussainDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0000-0001-8008-7262
Sandeep JhaDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0000-0001-7118-6293
Evelin BergerProteomics Core Facility, Sahlgrenska Academy, University of Gothenburg, 405 30 Gothenburg, Sweden.ORCID 0000-0002-6223-8845
Linnea MolanderDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Valentyna SevastianovaDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0000-0003-1216-4216
Zahra SheybaniDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Aaron Shekka EspinosaDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0000-0003-4336-5045
Ahmed ElmahdyDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Amin Al-AwarDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0000-0002-3199-2634
Yalda KakaeiDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Mana KalaniDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0009-0004-5180-3951
Ermir ZulfajDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Amirali NejatDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Abhishek JhaDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Tetiana PylovaDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0000-0002-6041-8690
Maryna KrasnikovaDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Erik Axel AnderssonDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.
Elmir OmerovicDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.ORCID 0000-0002-3875-8621
Björn RedforsDepartment of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, 413 45 Gothenburg, Sweden.

Funding

ALF Can be provider laterKonung Gustaf V:s och Drottning Victorias fond Can be provider laterSwedish Heart and Lung Foundation Can be provider laterSwedish Society of Medical Research Can be provider laterThe European Research Council Can be provider laterThe Swedish Research Council Can be provider later
6 · The paper itself

Abstract

backgroundST-elevation myocardial infarction (STEMI) and Takotsubo syndrome (TS) are two distinct cardiac conditions that both result in sudden loss of cardiac dysfunction and that are difficult to distinguish clinically. This study compared plasma protein changes in 24 women with STEMI and 12 women with TS in the acute phase (days 0-3 post symptom onset) and the stabilization phase (days 7, 14, and 30) to examine the molecular differences between these conditions.

methodsPlasma proteins from STEMI and TS patients were extracted during the acute and stabilization phases and analyzed via quantitative proteomics. Differential expression and functional significance were assessed. Data are accessible on ProteomeXchange, ID PXD051367.

resultsDuring the acute phase, STEMI patients showed higher levels of myocardial inflammation and tissue damage proteins compared to TS patients, along with reduced tissue repair and anti-inflammatory proteins. In the stabilization phase, STEMI patients exhibited ongoing inflammation and disrupted lipid metabolism. Notably, ADIPOQ was consistently downregulated in STEMI patients in both phases. When comparing the acute to the stabilization phase, STEMI patients showed increased inflammatory proteins and decreased structural proteins. Conversely, TS patients showed increased proteins involved in inflammation and the regulatory response to counter excessive inflammation. Consistent protein changes between the acute and stabilization phases in both conditions, such as SAA2, CRP, SAA1, LBP, FGL1, AGT, MAN1A1, APOA4, COMP, and PCOLCE, suggest shared underlying pathophysiological mechanisms.

conclusionsThis study presents protein changes in women with STEMI or TS and identifies ADIPOQ, SAA2, CRP, SAA1, LBP, FGL1, AGT, MAN1A1, APOA4, COMP, and PCOLCE as candidates for further exploration in both therapeutic and diagnostic contexts.

Indexed as

Blood ProteinsST Elevation Myocardial InfarctionTakotsubo CardiomyopathyAgedFemaleHumansMiddle AgedProteomicsBlood Proteinsbiomarkersenergy metabolismplasma proteomicsST-elevation myocardial infarctionTakotsubo syndrometemporal changestissue remodeling

Identifiers

PMID39513871
PMCPMC11545104

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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.