Evidence map›Paper›PMID 25177690›Full record

ReviewBioMed research international2014

Cardiovascular involvement in autoimmune diseases.

Jenny Amaya-Amaya, Laura Montoya-Sánchez, Adriana Rojas-Villarraga

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 6 pooled it
2.4field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 6 syntheses or guidelines pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Cardiovascular events risk in patients with systemic autoimmune diseases: a prognostic systematic review and meta-analysis.Clinical research in cardiology : official journal of the German Cardiac Society · 2024
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Autoantibodies in Atrial Fibrillation-State of the Art.International journal of molecular sciences · 2023
    Review
  14. The Role of Inflammation and Oxidative Stress in Rheumatic Heart Disease.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  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

3 authors at 1 institution in 1 country.

Jenny Amaya-AmayaCenter for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Carrera 24 No. 63C-69, 11001000 Bogotá, Colombia ; Mederi, Hospital Universitario Mayor, Calle 24 No. 29-45, 11001000 Bogotá, Colombia.
Laura Montoya-SánchezCenter for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Carrera 24 No. 63C-69, 11001000 Bogotá, Colombia ; Mederi, Hospital Universitario Mayor, Calle 24 No. 29-45, 11001000 Bogotá, Colombia.ORCID 0000-0001-5474-5970
Adriana Rojas-VillarragaCenter for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Carrera 24 No. 63C-69, 11001000 Bogotá, Colombia ; Mederi, Hospital Universitario Mayor, Calle 24 No. 29-45, 11001000 Bogotá, Colombia.ORCID 0000-0003-3145-2440
Hospital Universitario Nacional de Colombia · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune diseases (AD) represent a broad spectrum of chronic conditions that may afflict specific target organs or multiple systems with a significant burden on quality of life. These conditions have common mechanisms including genetic and epigenetics factors, gender disparity, environmental triggers, pathophysiological abnormalities, and certain subphenotypes. Atherosclerosis (AT) was once considered to be a degenerative disease that was an inevitable consequence of aging. However, research in the last three decades has shown that AT is not degenerative or inevitable. It is an autoimmune-inflammatory disease associated with infectious and inflammatory factors characterized by lipoprotein metabolism alteration that leads to immune system activation with the consequent proliferation of smooth muscle cells, narrowing arteries, and atheroma formation. Both humoral and cellular immune mechanisms have been proposed to participate in the onset and progression of AT. Several risk factors, known as classic risk factors, have been described. Interestingly, the excessive cardiovascular events observed in patients with ADs are not fully explained by these factors. Several novel risk factors contribute to the development of premature vascular damage. In this review, we discuss our current understanding of how traditional and nontraditional risk factors contribute to pathogenesis of CVD in AD.

Indexed as

Age DistributionAutoimmune DiseasesCardiovascular DiseasesCausalityComorbidityHumansIncidenceRheumatic DiseasesRisk FactorsScleroderma, SystemicSex Distribution

Identifiers

PMID25177690
PMCPMC4142566
OpenAlexW2165480863

What OpenQuestion holds

Textmetadata
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.