Evidence map›Paper›PMID 32228252›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2020

COVID-19, ACE2, and the cardiovascular consequences.

Andrew M South, Debra I Diz, Mark C Chappell

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 453 papers, 14 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
453citing papers in PubMed, 14 pooled it
18.2field-weighted citation impact, top 1% 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

453 citing papers in PubMed, 14 syntheses or guidelines pooled it, 793 citations in OpenAlex.

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393 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Andrew M SouthCardiovascular Sciences Center, Wake Forest School of Medicine, Winston-Salem, North Carolina.ORCID 0000-0002-3204-4142
Debra I DizCardiovascular Sciences Center, Wake Forest School of Medicine, Winston-Salem, North Carolina.
Mark C ChappellCardiovascular Sciences Center, Wake Forest School of Medicine, Winston-Salem, North Carolina.ORCID 0000-0001-5869-6037
Wake Forest University · US

Funding

Uric Acid, Klotho and Salt Sensitivity in Young Adults Born PretermR01HL146818 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C, SHALTOUT, HOSSAM · 2019 to 2023
$4.0M
Novel Angiotensin-(1-7) Endopeptidase in Fetal ProgrammingR21HD084227 · NICHD · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHAPPELL, MARK C, ROSE, JAMES C. · 2016 to 2017
$426k
NHLBI NIH HHS L40 HL148910NHLBI NIH HHS R01 HL146818NICHD NIH HHS R21 HD084227
6 · The paper itself

Abstract

The novel SARS coronavirus SARS-CoV-2 pandemic may be particularly deleterious to patients with underlying cardiovascular disease (CVD). The mechanism for SARS-CoV-2 infection is the requisite binding of the virus to the membrane-bound form of angiotensin-converting enzyme 2 (ACE2) and internalization of the complex by the host cell. Recognition that ACE2 is the coreceptor for the coronavirus has prompted new therapeutic approaches to block the enzyme or reduce its expression to prevent the cellular entry and SARS-CoV-2 infection in tissues that express ACE2 including lung, heart, kidney, brain, and gut. ACE2, however, is a key enzymatic component of the renin-angiotensin-aldosterone system (RAAS); ACE2 degrades ANG II, a peptide with multiple actions that promote CVD, and generates Ang-(1-7), which antagonizes the effects of ANG II. Moreover, experimental evidence suggests that RAAS blockade by ACE inhibitors, ANG II type 1 receptor antagonists, and mineralocorticoid antagonists, as well as statins, enhance ACE2 which, in part, contributes to the benefit of these regimens. In lieu of the fact that many older patients with hypertension or other CVDs are routinely treated with RAAS blockers and statins, new clinical concerns have developed regarding whether these patients are at greater risk for SARS-CoV-2 infection, whether RAAS and statin therapy should be discontinued, and the potential consequences of RAAS blockade to COVID-19-related pathologies such as acute and chronic respiratory disease. The current perspective critically examines the evidence for ACE2 regulation by RAAS blockade and statins, the cardiovascular benefits of ACE2, and whether ACE2 blockade is a viable approach to attenuate COVID-19.

Indexed as

Angiotensin-Converting Enzyme 2AnimalsBetacoronavirusCardiovascular DiseasesCoronavirus InfectionsCOVID-19HumansMalePandemicsPeptidyl-Dipeptidase APneumonia, ViralRatsRats, Inbred LewSARS-CoV-2Virus InternalizationACE2 protein, humanAce2 protein, ratAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase AACE2ANG IICOVID-19renin-angiotensin systemSARS-CoV-2statins

Identifiers

PMID32228252
PMCPMC7191628
OpenAlexW3013442544

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.