Evidence map›Paper›PMID 35203452›Full record

ReviewBiomedicines2022

Genetic Predisposition and Inflammatory Inhibitors in COVID-19: Where Do We Stand?

Marios Sagris, Panagiotis Theofilis, Alexios S Antonopoulos, Evangelos Oikonomou, Kostas Tsioufis, Dimitris Tousoulis

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Telomere Length: A Cardiovascular Biomarker and a Novel Therapeutic Target.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. 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

6 authors at 1 institution in 1 country.

Marios Sagris1st Cardiology Clinic, School of Medicine, "Hippokration" General Hospital, National and Kapodistrian University of Athens, 157 72 Athens, Greece.ORCID 0000-0002-3473-1368
Panagiotis Theofilis1st Cardiology Clinic, School of Medicine, "Hippokration" General Hospital, National and Kapodistrian University of Athens, 157 72 Athens, Greece.ORCID 0000-0001-9260-6306
Alexios S Antonopoulos1st Cardiology Clinic, School of Medicine, "Hippokration" General Hospital, National and Kapodistrian University of Athens, 157 72 Athens, Greece.
Evangelos Oikonomou1st Cardiology Clinic, School of Medicine, "Hippokration" General Hospital, National and Kapodistrian University of Athens, 157 72 Athens, Greece.ORCID 0000-0001-8079-0599
Kostas Tsioufis1st Cardiology Clinic, School of Medicine, "Hippokration" General Hospital, National and Kapodistrian University of Athens, 157 72 Athens, Greece.
Dimitris Tousoulis1st Cardiology Clinic, School of Medicine, "Hippokration" General Hospital, National and Kapodistrian University of Athens, 157 72 Athens, Greece.
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) and the resulting coronavirus disease-19 (COVID-19) have led to a global pandemic associated with high fatality rates. COVID-19 primarily manifests in the respiratory system as an acute respiratory distress syndrome following viral entry through the angiotensin-converting enzyme-2 (ACE2) that is present in pulmonary epithelial cells. Central in COVID-19 is the burst of cytokines, known as a "cytokine storm", and the subsequent widespread endothelial activation, leading to cardiovascular complications such as myocarditis, arrhythmias, and adverse vascular events, among others. Genetic alterations may play an additive, detrimental role in the clinical course of patients with COVID-19, since gene alterations concerning ACE2, major histocompatibility complex class I, and toll-like receptors may predispose patients to a worse clinical outcome. Since the role of inflammation is quintessential in COVID-19, pharmacologic inhibition of various signaling pathways such as the interleukin-1 and -6, tumor necrosis factor-alpha, interferon gamma, Janus kinase-signal transducer and activator of transcription, and granulocyte-macrophage colony-stimulating factor may ameliorate the prognosis following timely administration. Finally, frequently used, non-specific anti-inflammatory agents such as corticosteroids, statins, colchicine, and macrolides represent additional therapeutic considerations.

Indexed as

COVID-19cytokinesgeneticsinflammationSARS-CoV-2

Identifiers

PMID35203452
PMCPMC8868779
OpenAlexW4210821228

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.