Evidence map›Paper›PMID 35907817›Full record

ReviewCellular & molecular biology letters2022

Comprehensive overview of COVID-19-related respiratory failure: focus on cellular interactions.

Fahimeh Zamani Rarani, Mohammad Zamani Rarani, Michael R Hamblin, Bahman Rashidi, Seyed Mohammad Reza Hashemian, Hamed Mirzaei

Open access · goldAbstract readReview
In one paragraph

Review in Cellular & molecular biology letters, 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
1.4field-weighted citation impact, top 17% 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, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Nutrients · 2023
    Article
  8. Article
  9. Article
  10. Frontiers in microbiology · 2022
    Article
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 4 institutions in 2 countries.

Fahimeh Zamani RaraniDepartment of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Mohammad Zamani RaraniDepartment of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Michael R HamblinLaser Research Centre, Faculty of Health Science, University of Johannesburg, Doornfontein, 2028, South Africa.
Bahman RashidiDepartment of Anatomical Sciences, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. b_rashidi@med.mui.ac.ir.
Seyed Mohammad Reza HashemianChronic Respiratory Diseases Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran. smrhashemian@sbmu.ac.ir.
Hamed MirzaeiStudent Research Committee, Kashan University of Medical Sciences, Kashan, Iran. mirzaei-h@kaums.ac.ir.
Isfahan University of Medical Sciences · IRKashan University of Medical Sciences · IRMasih Daneshvari Hospital · IRUniversity of Johannesburg · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pandemic outbreak of coronavirus disease 2019 (COVID-19) has created health challenges in all parts of the world. Understanding the entry mechanism of this virus into host cells is essential for effective treatment of COVID-19 disease. This virus can bind to various cell surface molecules or receptors, such as angiotensin-converting enzyme 2 (ACE2), to gain cell entry. Respiratory failure and pulmonary edema are the most important causes of mortality from COVID-19 infections. Cytokines, especially proinflammatory cytokines, are the main mediators of these complications. For normal respiratory function, a healthy air-blood barrier and sufficient blood flow to the lungs are required. In this review, we first discuss airway epithelial cells, airway stem cells, and the expression of COVID-19 receptors in the airway epithelium. Then, we discuss the suggested molecular mechanisms of endothelial dysfunction and blood vessel damage in COVID-19. Coagulopathy can be caused by platelet activation leading to clots, which restrict blood flow to the lungs and lead to respiratory failure. Finally, we present an overview of the effects of immune and non-immune cells and cytokines in COVID-19-related respiratory failure.

Indexed as

COVID-19Respiratory InsufficiencyCytokinesHumansPeptidyl-Dipeptidase ASARS-CoV-2CytokinesPeptidyl-Dipeptidase AAirway epithelial cellsCOVID-19CytokinesEndothelial cellsPlateletsPulmonary edemaSARS-CoV-2

Identifiers

PMID35907817
PMCPMC9338538
OpenAlexW4288748803

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.