Evidence map›Paper›PMID 32460175›Full record

ReviewThrombosis research2020

The potential roles of Von Willebrand factor and neutrophil extracellular traps in the natural history of hypertrophic and hypertensive cardiomyopathy.

Richard C Becker, A Phillip Owens, Sakthivel Sadayappan

Abstract readReview
In one paragraph

Review in Thrombosis research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Causal atlas on comorbidities in cardiomyopathy: a Mendelian randomization study of European ancestry.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Article
  2. Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025
    Review
  3. Article
  4. 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

3 authors.

Richard C BeckerDivision of Cardiovascular Health and Disease, Heart, Lung and Blood Institute, University of Cincinnati College of Medicine, United States of America. Electronic address: richard.becker@uc.edu.
A Phillip OwensDivision of Cardiovascular Health and Disease, Heart, Lung and Blood Institute, University of Cincinnati College of Medicine, United States of America.
Sakthivel SadayappanDivision of Cardiovascular Health and Disease, Heart, Lung and Blood Institute, University of Cincinnati College of Medicine, United States of America.

Funding

Translational Research Skills Development Core (TRSDC): Training Future GeneratiU54HL112307 · NHLBI · DUKE UNIVERSITY · PI BECKER, RICHARD CLINTON · 2012 to 2016
$11.1M
IDENTIFYING NOVEL HEMOSTATIC PROTEINSR01HL065222 · NHLBI · DUKE UNIVERSITY · PI SULLENGER, BRUCE ALAN · 2000 to 2018
$7.9M
Fast myosin binding protein-C and cardiac contractility in heart failureR01HL105826 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2011 to 2025
$4.5M
The role of protease-activated receptor 2 (PAR2) in the pathogenesis of Alzheimer’s Disease (AD)R01HL141404 · NHLBI · UNIVERSITY OF CINCINNATI · PI OWENS III, ALBERT PHILLIP · 2018 to 2022
$2.4M
Skeletal Myosin-Binding Protein C (MyBP-C): Molecular Structure and FunctionR01AR067279 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CRAIG, ROGER W, WARSHAW, DAVID M · 2015 to 2019
$2.3M
IGF-2R is a new therapeutic target for cardiac ischemia-reperfusion injuryR01HL143490 · NHLBI · UNIVERSITY OF CINCINNATI · PI WANG, YIGANG · 2019 to 2022
$1.6M
Molecular mechanism of hypertrophic cardiomyopathy in populations of South Asian descendantsR01HL130356 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2016 to 2019
$1.6M
Myoarchitectural Basis of Heart FailureR56HL139680 · NHLBI · OCEAN STATE RESEARCH INSTITUTE, INC. · PI GILBERT, RICHARD J · 2018 to 2018
$431k
Fibrin(ogen) in Abdominal Aortic Aneurysm PathogenesisF31HL143987 · NHLBI · UNIVERSITY OF CINCINNATI · PI RUSSELL, HANNAH · 2018 to 2021
$121k
American Heart Association-American Stroke Association 15SFRN24110000NHLBI NIH HHS F31 HL143987NHLBI NIH HHS R01 HL065222NHLBI NIH HHS R01 HL105826NHLBI NIH HHS R01 HL130356NHLBI NIH HHS R01 HL141404NHLBI NIH HHS R01 HL143490NHLBI NIH HHS R56 HL139680NHLBI NIH HHS U54 HL112307NIAMS NIH HHS R01 AR067279
6 · The paper itself

Abstract

Inflammation is often applied broadly to human disease. Despite its general familiarity, inflammation is highly complex. There are numerous injurious, immune and infectious determinants, functional elements and signaling pathways, ranging from genetic to epigenetic, environmental, racial, molecular and cellular that participate in disease onset and progression, phenotypic heterogeneity, and treatment selection and response. In addition, inflammation can be tissue and organ specific, adding a layer of complexity to achieving a detailed and translatable understanding of its role in health and disease. The following review takes a close look at inflammation in the context of two common heart diseases, hypertrophic cardiomyopathy and hypertensive cardiomyopathy.

Indexed as

Cardiomyopathy, HypertrophicExtracellular TrapsHypertensionHumansInflammationvon Willebrand Factorvon Willebrand FactorHypertensive cardiomyopathyHypertrophic cardiomyopathyNeutrophil-derived extracellular trapsTissue-specific inflammationVon Willebrand factor

Identifiers

PMID32460175
PMCPMC7340095

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.