Evidence map›Paper›PMID 28779286›Full record

ReviewCurrent cardiology reports2017

Where Does Inflammation Fit?

Luigi M Biasucci, Giulio La Rosa, Daniela Pedicino, Alessia D'Aiello, Mattia Galli, Giovanna Liuzzo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current cardiology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  17. Antiplatelet therapy after percutaneous coronary intervention.EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology · 2022
    Article
  18. Article
  19. Molecular basis of acute coronary syndrome.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2022
    Review
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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 1 institution in 1 country.

Luigi M BiasucciDepartment of Cardiovascular Science, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168, Rome, Italy. lmbiasucci@virgilio.it.
Giulio La RosaDepartment of Cardiovascular Science, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168, Rome, Italy.
Daniela PedicinoDepartment of Cardiovascular Science, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168, Rome, Italy.
Alessia D'AielloDepartment of Cardiovascular Science, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168, Rome, Italy.
Mattia GalliDepartment of Cardiovascular Science, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168, Rome, Italy.
Giovanna LiuzzoDepartment of Cardiovascular Science, Catholic University of Sacred Heart, Largo Agostino Gemelli 8, 00168, Rome, Italy.
Agostino Gemelli University Polyclinic · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThis review focuses on the complex relationship between inflammation and the onset of acute coronary syndrome and heart failure. RECENT

findingsIn the last few years, two important lines of research brought new and essential information to light in the pathogenesis of acute coronary syndrome: a) the understanding of the immune mediate mechanisms of inflammation in Ischemic Heart Disease (IHD) and b) evidence that the inflammatory mechanisms associated with atherosclerosis and its complications can be modulated by anti-inflammatory molecules. A large amount of data also suggests that inflammation is a major component in the development and exacerbation of heart failure (HF), in a symbiotic relationship. In particular, recent evidence underlies peculiar aspects of the phenomenon: oxidative stress and autophagy; DAMPS and TLR-4 signaling activation; different macrophages lineage and the contribution of NLRP-3 inflammasome; adaptive immune system. A possible explanation that could unify the pathogenic mechanism of these different conditions is the rising evidence that increased bowel permeability may allow translation of gut microbioma product into the circulation. These findings clearly establish the role of inflammation as the great trigger for two of the major cardiovascular causes of death and morbidity. Further studies are needed, to better clarify the issue and to define more targeted approaches to reduce pathological inflammation while preserving the physiological one.

Indexed as

Acute Coronary SyndromeAtherosclerosisAutophagyCoronary Artery DiseaseGastrointestinal MicrobiomeHeart FailureHumansInflammasomesInflammationMacrophagesMyocardial IschemiaOxidative StressInflammasomesAcute coronary syndromeGut micrombiomaHeart failureImmune systemInflammation

Identifiers

PMID28779286
OpenAlexW2743957957

What OpenQuestion holds

Textmetadata
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.