Shuxun Ren

Oxidant stress from nitric oxide synthase-3 uncoupling stimulates cardiac pathologic remodeling from chronic pressure load.

p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes.

Overexpression of bone morphogenetic protein 10 in myocardium disrupts cardiac postnatal hypertrophic growth.

A novel mitochondrial matrix serine/threonine protein phosphatase regulates the mitochondria permeability transition pore and is essential for cellular survival and development.

Gi alpha 1-mediated cardiac electrophysiological remodeling and arrhythmia in hypertrophic cardiomyopathy.

Inducible and cardiac specific PTEN inactivation protects ischemia/reperfusion injury.

Post-translational regulation of calsarcin-1 during pressure overload-induced cardiac hypertrophy.

MAPK-activated protein kinase-2 in cardiac hypertrophy and cyclooxygenase-2 regulation in heart.

An accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria.

Absence of progeria-like disease phenotypes in knock-in mice expressing a non-farnesylated version of progerin.

Analysis of transcriptome complexity through RNA sequencing in normal and failing murine hearts.

Quantitative analysis of the chromatin proteome in disease reveals remodeling principles and identifies high mobility group protein B2 as a regulator of hypertrophic growth.

Endothelial deletion of murine Jag1 leads to valve calcification and congenital heart defects associated with Alagille syndrome.

Systems proteomics of cardiac chromatin identifies nucleolin as a regulator of growth and cellular plasticity in cardiomyocytes.

IRE1 phosphatase PP2Ce regulates adaptive ER stress response in the postpartum mammary gland.

Mapping genetic contributions to cardiac pathology induced by Beta-adrenergic stimulation in mice.

Titration of mitochondrial fusion rescues Mff-deficient cardiomyopathy.

DNA Methylation Indicates Susceptibility to Isoproterenol-Induced Cardiac Pathology and Is Associated With Chromatin States.

Genetic Dissection of Cardiac Remodeling in an Isoproterenol-Induced Heart Failure Mouse Model.

The long noncoding RNA Chaer defines an epigenetic checkpoint in cardiac hypertrophy.

The chromatin-binding protein Smyd1 restricts adult mammalian heart growth.

Systems Genetics Approach Identifies Gene Pathways and Adamts2 as Drivers of Isoproterenol-Induced Cardiac Hypertrophy and Cardiomyopathy in Mice.

Cardiac myocyte p38α kinase regulates angiogenesis via myocyte-endothelial cell cross-talk during stress-induced remodeling in the heart.

High-Resolution Mapping of Chromatin Conformation in Cardiac Myocytes Reveals Structural Remodeling of the Epigenome in Heart Failure.

A personalized, multiomics approach identifies genes involved in cardiac hypertrophy and heart failure.

Humanin analog enhances the protective effect of dexrazoxane against doxorubicin-induced cardiotoxicity.

Systems Genetics Approach to Biomarker Discovery: GPNMB and Heart Failure in Mice and Humans.

RBFox2-miR-34a-Jph2 axis contributes to cardiac decompensation during heart failure.

Glucagon Receptor Antagonism Ameliorates Progression of Heart Failure.