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Circulation Research|April 22, 2021
NAD+ Repletion Reverses Heart Failure With Preserved Ejection FractionDan Tong, Gabriele G Schiattarella, Nan Jiang, et al.Frontiers in Physiology|September 14, 2018
The Fibrotic Substrate in Persistent Atrial Fibrillation Patients: Comparison Between Predictions From Computational Modeling and Measurements From Focal Impulse and Rotor MappingPatrick M Boyle, Joe B Hakim, Sohail Zahid, et al.Circulation|December 2, 2011
Pulmonary capillary wedge pressure augments right ventricular pulsatile loadingRyan J Tedford, Paul M Hassoun, Stephen C Mathai, et al.Biomarkers : Biochemical Indicators of Exposure, Response, and Susceptibility to Chemicals|March 15, 2021
Cyclic guanosine monophosphate and 10-year change in left ventricular mass: the Multi-Ethnic Study of Atherosclerosis (MESA)Vinita Subramanya, Di Zhao, Pamela Ouyang, et al.Journal of Molecular and Cellular Cardiology|May 7, 2013
Anti-hypertrophic and anti-oxidant effect of beta3-adrenergic stimulation in myocytes requires differential neuronal NOS phosphorylationVabren L Watts, Fernando M Sepulveda, Oscar H Cingolani, et al.Annals of Neurology|July 22, 2014
Sildenafil does not improve cardiomyopathy in Duchenne/Becker muscular dystrophyDoris G Leung, Daniel A Herzka, W Reid Thompson, et al.Pulmonary Circulation|June 12, 2015
Right ventricular remodeling in idiopathic and scleroderma-associated pulmonary arterial hypertension: two distinct phenotypesBenjamin W Kelemen, Stephen C Mathai, Ryan J Tedford, et al.Circulation Research|April 3, 2004
Role of cardiac myosin binding protein C in sustaining left ventricular systolic stiffeningBradley M Palmer, Dimitrios Georgakopoulos, Paul M Janssen, et al.Journal of Molecular and Cellular Cardiology|February 5, 2011
RGS2 is a primary terminator of β₂-adrenergic receptor-mediated G(i) signalingKhalid Chakir, Weizhong Zhu, Sharon Tsang, et al.Proceedings of the National Academy of Sciences of the United States of America|January 24, 2014
Combined TRPC3 and TRPC6 blockade by selective small-molecule or genetic deletion inhibits pathological cardiac hypertrophyKinya Seo, Peter P Rainer, Virginia Shalkey Hahn, et al.Pageof 40