Evidence map›Paper›PMID 34195965›Full record

ReviewReviews in endocrine & metabolic disorders2022

Functional ACE2 deficiency leading to angiotensin imbalance in the pathophysiology of COVID-19.

Joshua R Cook, John Ausiello

Open access · bronzeAbstract readReview
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Diabetic Ketoacidosis and Long-term Insulin Requirements in Youths with Newly Diagnosed Type 2 Diabetes During the SARS-CoV-2 Pandemic.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2023
    Article
  6. Article
  7. Observational
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Molecular pathways involved in COVID-19 and potential pathway-based therapeutic targets.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  16. Mechanisms of SARS-CoV-2 Infection-Induced Kidney Injury: A Literature Review.Frontiers in cellular and infection microbiology · 2022
    Review
  17. 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

2 authors at 1 institution in 1 country.

Joshua R CookNew York-Presbyterian Hospital and the Columbia University Irving Medical Center, New York, NY, USA.ORCID 0000-0001-6004-0504
John AusielloNew York-Presbyterian Hospital and the Columbia University Irving Medical Center, New York, NY, USA. ja2395@cumc.columbia.edu.ORCID 0000-0003-2097-6839
NewYork–Presbyterian Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SARS-CoV-2, the virus responsible for COVID-19, uses angiotensin converting enzyme 2 (ACE2) as its primary cell-surface receptor. ACE2 is a key enzyme in the counter-regulatory pathway of the broader renin-angiotensin system (RAS) that has been implicated in a broad array of human pathology. The RAS is composed of two competing pathways that work in opposition to each other: the "conventional" arm involving angiotensin converting enzyme (ACE) generating angiotensin-2 and the more recently identified ACE2 pathway that generates angiotensin (1-7). Following the original SARS pandemic, additional studies suggested that coronaviral binding to ACE2 resulted in downregulation of the membrane-bound enzyme. Given the similarities between the two viruses, many have posited a similar process with SARS-CoV-2. Proponents of this ACE2 deficiency model argue that downregulation of ACE2 limits its enzymatic function, thereby skewing the delicate balance between the two competing arms of the RAS. In this review we critically examine this model. The available data remain incomplete but are consistent with the possibility that the broad multisystem dysfunction of COVID-19 is due in large part to functional ACE2 deficiency leading to angiotensin imbalance with consequent immune dysregulation and endothelial cell dysfunction.

Indexed as

Angiotensin-Converting Enzyme 2AngiotensinsCOVID-19HumansPandemicsRenin-Angiotensin SystemSARS-CoV-2ACE2 protein, humanAngiotensin-Converting Enzyme 2AngiotensinsAngiotensin 1–7Angiotensin-2Angiotensin converting enzymeAngiotensin converting enzyme 2Renin angiotensin system

Identifiers

PMID34195965
PMCPMC8245275
OpenAlexW3173609475

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.