Evidence map›Paper›PMID 32448590›Full record

ArticleMayo Clinic proceedings2020

Marked Up-Regulation of ACE2 in Hearts of Patients With Obstructive Hypertrophic Cardiomyopathy: Implications for SARS-CoV-2-Mediated COVID-19.

J Martijn Bos, Virginia B Hebl, Ann L Oberg, Zhifu Sun, Daniel S Herman, Polakit Teekakirikul, Jonathan G Seidman, Christine E Seidman, Cristobal G Dos Remedios, Joseph J Maleszewski and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Mayo Clinic proceedings, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
9.5field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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  17. SARS-CoV-2 attacks the weakest point - COVID-19 course in a pediatric patient with Friedreich's ataxia.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022
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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

17 authors at 6 institutions in 2 countries.

J Martijn BosDepartment of Molecular Pharmacology & Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory, Mayo Clinic, Rochester, MN.
Virginia B HeblDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN.
Ann L ObergDivision of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN.
Zhifu SunDivision of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN.
Daniel S HermanDepartment of Genetics, Harvard Medical School, Boston, MA.
Polakit TeekakirikulDepartment of Genetics, Harvard Medical School, Boston, MA.
Jonathan G SeidmanDepartment of Genetics, Harvard Medical School, Boston, MA.
Christine E SeidmanDepartment of Genetics, Harvard Medical School, Boston, MA; Cardiovascular Division, Brigham and Women's Hospital, Boston, MA; Howard Hughes Medical Institute, Chevy Chase, MD.
Cristobal G Dos RemediosMechanobiology Laboratory, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.
Joseph J MaleszewskiDepartment of Laboratory Medicine & Pathology, Mayo Clinic, Rochester, MN.
Hartzell V SchaffDepartment of Cardiovascular Surgery, Mayo Clinic, Rochester, MN.
Joseph A DearaniDepartment of Cardiovascular Surgery, Mayo Clinic, Rochester, MN.
Peter A NoseworthyDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN.
Paul A FriedmanDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN.
Steve R OmmenDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN.
Frank V BrozovichDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, MN.
Michael J AckermanDepartment of Molecular Pharmacology & Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory, Mayo Clinic, Rochester, MN; Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN; Division of Pediatric Cardiology, Department of Pediatric and Adolescent Medicine, Windland Smith Rice Genetic Heart Rhythm Clinic, Mayo Clinic, Rochester, MN. Electronic address: ackerman.michael@mayo.edu.
Mayo Clinic in Arizona · USHarvard University · USMayo Clinic · USMayo Clinic in Florida · USBrigham and Women's Hospital · USVictor Chang Cardiac Research Institute · AU

Funding

Molecular Signaling in Hypertrophic CardiomyopathyR01HL084553 · NHLBI · HARVARD MEDICAL SCHOOL · PI SEIDMAN, JONATHAN G · 2007 to 2022
$5.9M
Genetic Determinants of Chagas CardiomyopathyR01HL133165 · NHLBI · HARVARD MEDICAL SCHOOL · PI SEIDMAN, CHRISTINE E · 2017 to 2020
$1.7M
NHLBI NIH HHS R01 HL084553NHLBI NIH HHS R01 HL133165
6 · The paper itself

Abstract

objectiveTo explore the transcriptomic differences between patients with hypertrophic cardiomyopathy (HCM) and controls. PATIENTS AND

methodsRNA was extracted from cardiac tissue flash frozen at therapeutic surgical septal myectomy for 106 patients with HCM and 39 healthy donor hearts. Expression profiling of 37,846 genes was performed using the Illumina Human HT-12v3 Expression BeadChip. All patients with HCM were genotyped for pathogenic variants causing HCM. Technical validation was performed using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. This study was started on January 1, 1999, and final analysis was completed on April 20, 2020.

resultsOverall, 22% of the transcriptome (8443 of 37,846 genes) was expressed differentially between HCM and control tissues. Analysis by genotype revealed that gene expression changes were similar among genotypic subgroups of HCM, with only 4% (1502 of 37,846) to 6% (2336 of 37,846) of the transcriptome exhibiting differential expression between genotypic subgroups. The qRT-PCR confirmed differential expression in 92% (11 of 12 genes) of tested transcripts. Notably, in the context of coronavirus disease 2019 (COVID-19), the transcript for angiotensin I converting enzyme 2 (ACE2), a negative regulator of the angiotensin system, was the single most up-regulated gene in HCM (fold-change, 3.53; q-value =1.30×10

conclusionMore than 20% of the transcriptome is expressed differentially between HCM and control tissues. Importantly, ACE2 was the most up-regulated gene in HCM, indicating perhaps the heart's compensatory effort to mount an antihypertrophic, antifibrotic response. However, given that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses ACE2 for viral entry, this 5-fold increase in ACE2 protein may confer increased risk for COVID-19 manifestations and outcomes in patients with increased ACE2 transcript expression and protein levels in the heart.

Indexed as

BetacoronavirusAdolescentAdultAgedAngiotensin-Converting Enzyme 2Cardiomyopathy, HypertrophicCase-Control StudiesChildCoronavirus InfectionsCOVID-19GenotypeHumansMiddle AgedMyocardiumPandemicsPeptidyl-Dipeptidase AACE2 protein, humanAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase ARNA, Messenger

Identifiers

PMID32448590
PMCPMC7186205
OpenAlexW3018815390

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.