Nature Communications (Jun 2019)
Pathologic gene network rewiring implicates PPP1R3A as a central regulator in pressure overload heart failure
- Pablo Cordero,
- Victoria N. Parikh,
- Elizabeth T. Chin,
- Ayca Erbilgin,
- Michael J. Gloudemans,
- Ching Shang,
- Yong Huang,
- Alex C. Chang,
- Kevin S. Smith,
- Frederick Dewey,
- Kathia Zaleta,
- Michael Morley,
- Jeff Brandimarto,
- Nicole Glazer,
- Daryl Waggott,
- Aleksandra Pavlovic,
- Mingming Zhao,
- Christine S. Moravec,
- W. H. Wilson Tang,
- Jamie Skreen,
- Christine Malloy,
- Sridhar Hannenhalli,
- Hongzhe Li,
- Scott Ritter,
- Mingyao Li,
- Daniel Bernstein,
- Andrew Connolly,
- Hakon Hakonarson,
- Aldons J. Lusis,
- Kenneth B. Margulies,
- Anna A. Depaoli-Roach,
- Stephen B. Montgomery,
- Matthew T. Wheeler,
- Thomas Cappola,
- Euan A. Ashley
Affiliations
- Pablo Cordero
- Division of Cardiovascular Medicine, Stanford University
- Victoria N. Parikh
- Division of Cardiovascular Medicine, Stanford University
- Elizabeth T. Chin
- Division of Cardiovascular Medicine, Stanford University
- Ayca Erbilgin
- Division of Cardiovascular Medicine, Stanford University
- Michael J. Gloudemans
- Biomedical Informatics Program, Stanford University
- Ching Shang
- Division of Cardiovascular Medicine, Stanford University
- Yong Huang
- Division of Cardiovascular Medicine, Stanford University
- Alex C. Chang
- Division of Cardiovascular Medicine, Stanford University
- Kevin S. Smith
- Department of Pathology, Stanford University
- Frederick Dewey
- Division of Cardiovascular Medicine, Stanford University
- Kathia Zaleta
- Division of Cardiovascular Medicine, Stanford University
- Michael Morley
- Division of Cardiology, University of Pennsylvania
- Jeff Brandimarto
- Department of Medicine, University of Pennsylvania
- Nicole Glazer
- Department of Medicine, Boston University School of Medicine
- Daryl Waggott
- Division of Cardiovascular Medicine, Stanford University
- Aleksandra Pavlovic
- Division of Cardiovascular Medicine, Stanford University
- Mingming Zhao
- Department of Pediatrics, Stanford University
- Christine S. Moravec
- Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute
- W. H. Wilson Tang
- Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute
- Jamie Skreen
- Providence Medical Group—Milwaukie
- Christine Malloy
- Center for Bioinformatics and Computational Biology, University of Maryland
- Sridhar Hannenhalli
- Center for Bioinformatics and Computational Biology, University of Maryland
- Hongzhe Li
- Biostatistics and Epidemiology, University of Pennsylvania
- Scott Ritter
- Division of Cardiology, University of Pennsylvania
- Mingyao Li
- Biostatistics and Epidemiology, University of Pennsylvania
- Daniel Bernstein
- Department of Pediatrics, Stanford University
- Andrew Connolly
- Department of Pathology, University of California San Francisco
- Hakon Hakonarson
- Department of Pediatrics, The Children’s Hospital of Philadelphia
- Aldons J. Lusis
- Departments of Medicine, University of California Los Angeles
- Kenneth B. Margulies
- Division of Cardiology, University of Pennsylvania
- Anna A. Depaoli-Roach
- School of Medicine, Indiana University
- Stephen B. Montgomery
- Department of Pathology, Stanford University
- Matthew T. Wheeler
- Division of Cardiovascular Medicine, Stanford University
- Thomas Cappola
- Division of Cardiology, University of Pennsylvania
- Euan A. Ashley
- Division of Cardiovascular Medicine, Stanford University
- DOI
- https://doi.org/10.1038/s41467-019-10591-5
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 14
Abstract
The genetic and pathogenetic basis of heart failure is incompletely understood. Here, the authors present a high-fidelity tissue collection from rapidly preserved failing and non-failing control hearts which are used for eQTL mapping and network analysis, resulting in the prioritization of PPP1R3A as a heart failure gene.
