Evidence map›Paper›PMID 33443121›Full record

ReviewOpen heart2020

Manipulation of ACE2 expression in COVID-19.

Farhan Chaudhry, Sergio Lavandero, Xiang Xie, Basera Sabharwal, Ying-Ying Zheng, Ashish Correa, Jagat Narula, Phillip Levy

Open access · goldAbstract readComparative StudyReview
In one paragraph

Review in Open heart, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
1.6field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Expression ofBiomedical reports · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. A Natural Bioactive Peptide fromInternational journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

8 authors at 4 institutions in 3 countries.

Farhan ChaudhryDepartment of Emergency Medicine and Integrative Biosciences Center, Wayne State University School of Medicine, Detroit, Michigan, USA gf9603@wayne.edu.ORCID 0000-0003-0951-7279
Sergio LavanderoAdvanced Center for Chronic Diseases (ACCDiS), Facultad de Ciencias Quimicas y Farmaceuticas and Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Xiang XieDepartment of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, China.ORCID 0000-0002-0632-4626
Basera SabharwalDivision of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Ying-Ying ZhengDepartment of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, China.
Ashish CorreaDivision of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Jagat NarulaDivision of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Phillip LevyDepartment of Emergency Medicine and Integrative Biosciences Center, Wayne State University School of Medicine, Detroit, Michigan, USA.
Icahn School of Medicine at Mount Sinai · USWayne State University · USXinjiang Medical University · CNAdvanced Center for Chronic Diseases · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SARS-CoV-2 is the virus responsible for the ongoing COVID-19 outbreak. The virus uses ACE2 receptor for viral entry. ACE2 is part of the counter-regulatory renin-angiotensin-aldosterone system and is also expressed in the lower respiratory tract along the alveolar epithelium. There is, however, significant controversy regarding the role of ACE2 expression in COVID-19 pathogenesis. Some have argued that decreasing ACE2 expression would result in decreased susceptibility to the virus by decreasing available binding sites for SARS-CoV-2 and restricting viral entry into the cells. Others have argued that, like the pathogenesis of other viral pneumonias, including those stemming from previous severe acute respiratory syndrome (SARS) viruses, once SARS-CoV-2 binds to ACE2, it downregulates ACE2 expression. Lack of the favourable effects of ACE2 might exaggerate lung injury by a variety of mechanisms. In order to help address this controversy, we conducted a literature search and review of relevant preclinical and clinical publications pertaining to SARS-CoV-2, COVID-19, ACE2, viral pneumonia, SARS, acute respiratory distress syndrome and lung injury. Our review suggests, although controversial, that patients at increased susceptibility to COVID-19 complications may have reduced baseline ACE2, and by modulating ACE2 expression one can possibly improve COVID-19 outcomes. Herein, we elucidate why and how this potential mechanism might work.

Indexed as

AdultAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsAnimalsCOVID-19COVID-19 Drug TreatmentDown-RegulationFemaleHumansImmunityLung InjuryMaleMiceMiddle AgedModels, AnimalAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor Antagonistshypertensionintensive carelung injury

Identifiers

PMID33443121
PMCPMC7757413
OpenAlexW3117681590

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.