Evidence map›Paper›PMID 33348925›Full record

ReviewInternational journal of molecular sciences2020

From Brain to Heart: Possible Role of Amyloid-β in Ischemic Heart Disease and Ischemia-Reperfusion Injury.

Giulia Gagno, Federico Ferro, Alessandra Lucia Fluca, Milijana Janjusevic, Maddalena Rossi, Gianfranco Sinagra, Antonio Paolo Beltrami, Rita Moretti, Aneta Aleksova

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Alterations in the inflammatory homeostasis of aging-related cardiac dysfunction and Alzheimer's diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  7. Review
  8. Trajectory of Cardiogenic Dementia: A New Perspective.Journal of cellular and molecular medicine · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. MCardiovascular diagnosis and therapy · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  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

9 authors at 2 institutions in 1 country.

Giulia GagnoCardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina (ASUGI) and University of Trieste, 34100 Trieste, Italy.
Federico FerroCardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina (ASUGI) and University of Trieste, 34100 Trieste, Italy.
Alessandra Lucia FlucaCardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina (ASUGI) and University of Trieste, 34100 Trieste, Italy.
Milijana JanjusevicCardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina (ASUGI) and University of Trieste, 34100 Trieste, Italy.
Maddalena RossiCardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina (ASUGI) and University of Trieste, 34100 Trieste, Italy.
Gianfranco SinagraCardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina (ASUGI) and University of Trieste, 34100 Trieste, Italy.
Antonio Paolo BeltramiDepartment of Medicine (DAME), University of Udine, 33100 Udine, Italy.ORCID 0000-0002-0679-2710
Rita MorettiDepartment of Internal Medicine and Neurology, Neurological Clinic, 34100 Trieste, Italy.ORCID 0000-0002-9731-2697
Aneta AleksovaCardiothoracovascular Department, Azienda Sanitaria Universitaria Giuliano Isontina (ASUGI) and University of Trieste, 34100 Trieste, Italy.ORCID 0000-0001-7711-9905
University of Trieste · ITUniversity of Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic heart disease (IHD) is among the leading causes of death in developed countries. Its pathological origin is traced back to coronary atherosclerosis, a lipid-driven immuno-inflammatory disease of the arteries that leads to multifocal plaque development. The primary clinical manifestation of IHD is acute myocardial infarction (AMI),) whose prognosis is ameliorated with optimal timing of revascularization. Paradoxically, myocardium re-perfusion can be detrimental because of ischemia-reperfusion injury (IRI), an oxidative-driven process that damages other organs. Amyloid-β (Aβ) plays a physiological role in the central nervous system (CNS). Alterations in its synthesis, concentration and clearance have been connected to several pathologies, such as Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA). Aβ has been suggested to play a role in the pathogenesis of IHD and cerebral IRI. The purpose of this review is to summarize what is known about the pathological role of Aβ in the CNS; starting from this evidence, we will illustrate the role played by Aβ in the development of coronary atherosclerosis and its possible implications in the pathophysiology of IHD and myocardial IRI. Better elucidation of Aβ's contribution to the molecular pathways underlying IHD and IRI could be of great help in developing new therapeutic strategies.

Indexed as

Amyloid beta-PeptidesAnimalsBrainHeartHumansMyocardial IschemiaReperfusion InjuryAmyloid beta-PeptidesAlzheimer’s diseaseamyloid betaatherosclerosisAβ1-40BACE1cardiovascular mortalitycerebral amyloid angiopathyischemia-reperfusion injuryischemic heart diseasemyocardial infarction

Identifiers

PMID33348925
PMCPMC7766370
OpenAlexW3113023657

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.