Evidence map›Paper›PMID 33454213›Full record

ReviewHeart, lung & circulation2021

The Counter Regulatory Axis of the Lung Renin-Angiotensin System in Severe COVID-19: Pathophysiology and Clinical Implications.

Filippos Triposkiadis, Randall C Starling, Andrew Xanthopoulos, Javed Butler, Harisios Boudoulas

Open access · bronzeAbstract readReview
In one paragraph

Review in Heart, lung & circulation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.4field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  5. COVID-19 and the heart.World journal of clinical cases · 2022
    Review
  6. COVID-19, vaccines and deficiency of ACEEuropean journal of internal medicine · 2022
    Review
  7. Proline-specific peptidase activities (DPP4, PRCP, FAP and PREP) in plasma of hospitalized COVID-19 patients.Clinica chimica acta; international journal of clinical chemistry · 2022
    Article
  8. Review
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  10. Article
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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

5 authors at 4 institutions in 2 countries.

Filippos TriposkiadisDepartment of Cardiology, Larissa University General Hospital, Larissa, Greece. Electronic address: ftriposkiadis@gmail.com.
Randall C StarlingKaufman Center for Heart Failure and Recovery, Heart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA.
Andrew XanthopoulosDepartment of Cardiology, Larissa University General Hospital, Larissa, Greece.
Javed ButlerDepartment of Medicine, University of Mississippi, Jackson, MS, USA.
Harisios BoudoulasDepartment of Medicine/Cardiovascular Medicine, The Ohio State University, Columbus, OH, USA.
University Hospital of Larissa · GRCleveland Clinic · USThe Ohio State University · USUniversity of Mississippi · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severe acute respiratory syndrome coronavirus (SARS-CoV)-2, which is responsible for coronavirus disease 2019 (COVID-19), uses angiotensin (ANG)-converting enzyme 2 (ACE2) as the entrance receptor. Although most COVID-19 cases are mild, some are severe or critical, predominantly due to acute lung injury. It has been widely accepted that a counter regulatory renin-angiotensin system (RAS) axis including the ACE2/ANG [1-7]/Mas protects the lungs from acute lung injury. However, recent evidence suggests that the generation of protective ANG [1-7] in the lungs is predominantly mediated by proinflammatory prolyl oligopeptidase (POP), which has been repeatedly demonstrated to be involved in lung pathology. This review contends that acute lung injury in severe COVID-19 is characterised by a) ACE2 downregulation and malfunction (inflammatory signalling) due to viral occupation, and b) dysregulation of the protective RAS axis, predominantly due to increased activity of proinflammatory POP. It follows that a reasonable treatment strategy in COVID-19-related acute lung injury would be delivering functional recombinant (r) ACE2 forms to trap the virus. Additionally, or alternatively to rACE2 delivery, the potential benefits resulting from lowering POP activity should also be explored. These treatment strategies deserve further investigation.

Indexed as

Acute Lung InjuryCOVID-19Signal TransductionAngiotensin-Converting Enzyme 2Down-RegulationDrug DiscoveryHumansRenin-Angiotensin SystemSARS-CoV-2ACE2 protein, humanAngiotensin-Converting Enzyme 2Acute lung injuryCoronavirus disease 2019Renin-angiotensin system

Identifiers

PMID33454213
PMCPMC7831862
OpenAlexW3111870298

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.