Evidence map›Paper›PMID 25032197›Full record

ReviewWorld journal of clinical cases2014

Infectious burden and atherosclerosis: A clinical issue.

Rosa Sessa, Marisa Di Pietro, Simone Filardo, Ombretta Turriziani

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of clinical cases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
14.9field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Medicina (Kaunas, Lithuania) · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. The Detection ofPathogens (Basel, Switzerland) · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
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  18. Article
  19. Clots retrieved by mechanical thrombectomy from acute ischemic stroke patients show no evidence of bacteria.Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences · 2019
    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

4 authors at 1 institution in 1 country.

Rosa SessaRosa Sessa, Marisa Di Pietro, Simone Filardo, Department of Public Health and Infectious Diseases, "Sapienza" University, 00185 Rome, Italy.
Marisa Di PietroRosa Sessa, Marisa Di Pietro, Simone Filardo, Department of Public Health and Infectious Diseases, "Sapienza" University, 00185 Rome, Italy.
Simone FilardoRosa Sessa, Marisa Di Pietro, Simone Filardo, Department of Public Health and Infectious Diseases, "Sapienza" University, 00185 Rome, Italy.
Ombretta TurrizianiRosa Sessa, Marisa Di Pietro, Simone Filardo, Department of Public Health and Infectious Diseases, "Sapienza" University, 00185 Rome, Italy.
Department of Public Health · MM

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerotic cardiovascular diseases, chronic inflammatory diseases of multifactorial etiology, are the leading cause of death worldwide. In the last decade, more infectious agents, labeled as "infectious burden", rather than any single pathogen, have been showed to contribute to the development of atherosclerosis through different mechanisms. Some microorganisms, such as Chlamydia pneumoniae (C. pneumoniae), human cytomegalovirus, etc. may act directly on the arterial wall contributing to endothelial dysfunction, foam cell formation, smooth muscle cell proliferation, platelet aggregation as well as cytokine, reactive oxygen specie, growth factor, and cellular adhesion molecule production. Others, such as Helicobacter pylori (H. pylori), influenza virus, etc. may induce a systemic inflammation which in turn may damage the vascular wall (e.g., by cytokines and proteases). Moreover, another indirect mechanism by which some infectious agents (such as H. pylori, C. pneumoniae, periodontal pathogens, etc.) may play a role in the pathogenesis of atherosclerosis is molecular mimicry. Given the complexity of the mechanisms by which each microorganism may contribute to atherosclerosis, defining the interplay of more infectious agents is far more difficult because the pro-atherogenic effect of each pathogen might be amplified. Clearly, continued research and a greater awareness will be helpful to improve our knowledge on the complex interaction between the infectious burden and atherosclerosis.

Indexed as

AtherosclerosisBacteriaInfectious burdenPathogenetic mechanismsVirus

Identifiers

PMID25032197
PMCPMC4097149
OpenAlexW2005975267

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.