Evidence map›Paper›PMID 34305426›Full record

ReviewSaudi journal of biological sciences2021

RAAS, ACE2 and COVID-19; a mechanistic review.

Ahmed Elshafei, Emad Gamil Khidr, Ahmed A El-Husseiny, Maher H Gomaa

Open access · hybridAbstract readReview
In one paragraph

Review in Saudi journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ACE2: Friend or Foe in Post-COVID-19 Neurodegeneration?International journal of molecular sciences · 2025
    Review
  5. Article
  6. Observational
  7. Article
  8. Review
  9. The effect of adrenalectomy on bleomycin-induced pulmonary fibrosis in mice.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  10. A New Biomarker Copeptin in Determining Disease Severity in COVID-19.Infectious diseases & clinical microbiology · 2024
    Article
  11. The prognostic significance of insulin resistance in COVID-19: a review.Journal of diabetes and metabolic disorders · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mutations in SARS-CoV-2: Insights on structure, variants, vaccines, and biomedical interventions.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Review
  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

4 authors at 1 institution in 1 country.

Ahmed ElshafeiBiochemistry and Molecular Biology Department, Faculty of Pharmacy, Al-Azhar University, Nasr City 11231, Cairo, Egypt.
Emad Gamil KhidrBiochemistry and Molecular Biology Department, Faculty of Pharmacy, Al-Azhar University, Nasr City 11231, Cairo, Egypt.
Ahmed A El-HusseinyBiochemistry and Molecular Biology Department, Faculty of Pharmacy, Al-Azhar University, Nasr City 11231, Cairo, Egypt.
Maher H GomaaBiochemistry and Molecular Biology Department, Faculty of Pharmacy, Al-Azhar University, Nasr City 11231, Cairo, Egypt.
Al-Azhar University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) in coronavirus disease 2019 (COVID-19) patients has been claimed as associated with the risk of COVID-19 infection and its subsequent morbidities and mortalities. These claims were resulting from the possibility of upregulating the expression of angiotensin-converting enzyme 2 (ACE2), facilitation of SARS-CoV-2 entry, and increasing the susceptibility of infection in such treated cardiovascular patients. ACE2 and renin-angiotensin-aldosterone system (RAAS) products have a critical function in controlling the severity of lung injury, fibrosis, and failure following the initiation of the disease. This review is to clarify the mechanisms beyond the possible deleterious effects of angiotensin II (Ang II), and the potential protective role of angiotensin 1-7 (Ang 1-7) against pulmonary fibrosis, with a subsequent discussion of the latest updates on ACEIs/ARBs use and COVID-19 susceptibility in the light of these mechanisms and biochemical explanation.

Indexed as

ACE1, angiotensin-converting enzyme 1ACE2ACE2, angiotensin-converting enzyme 2ACEIsACEIs, angiotensin-converting enzyme inhibitorsAEC-II, alveolar epithelial type II cellsAng 1-7, angiotensin 1-7Ang 1-9, angiotensin 1-9AngI, angiotensin IAngII, angiotensin IIAngiotensin 1–7Angiotensin IIARBsARBs, angiotensin receptor blockersAT1R, angiotensin type 1 receptorAT2R, angiotensin type 2 receptorCOVID-19COVID-19, coronavirus disease 2019CVD, cardiovascular diseaseERK, extracellular signal-regulated kinaseICU, intensive care unitMAPK, mitogen-activated protein kinasemiR-21, microRNA-21NLRP3, (NOD, LRR, and pyrin domain-containing protein 3)RAAS, renin-angiotensin-aldosterone systemTGF-β, transforming growth factor-beta

Identifiers

PMID34305426
PMCPMC8270731
OpenAlexW3181297434

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.