Circulation Research Editors’ Annual Report for 2005
GDF15, a Cardioprotective TGF-β Superfamily Protein
A Female Way to Protect the Heart
MAPK = Mitogen-Activated Protein KChIP2?
Novel Faces to Old Friends
Organizing Motility
Proteomics of the Heart
Rho Kinases in Cardiovascular Physiology and Pathophysiology
Direct Interaction of the Cell Division Cycle 37 Homolog Inhibits Endothelial Nitric Oxide Synthase Activity
GDF15/MIC-1 Functions As a Protective and Antihypertrophic Factor Released From the Myocardium in Association With SMAD Protein Activation
The Transforming Growth Factor-β Superfamily Member Growth-Differentiation Factor-15 Protects the Heart From Ischemia/Reperfusion Injury
Acute Antiinflammatory Properties of Statins Involve Peroxisome Proliferator–Activated Receptor-α via Inhibition of the Protein Kinase C Signaling Pathway
Inhibition of Versican Synthesis by Antisense Alters Smooth Muscle Cell Phenotype and Induces Elastic Fiber Formation In Vitro and in Neointima After Vessel Injury
LPP Expression During In Vitro Smooth Muscle Differentiation and Stent-Induced Vascular Injury
Mitogen-Activated Protein Kinases Control Cardiac KChIP2 Gene Expression
Endothelial Cell Cortactin Phosphorylation by Src Contributes to Polymorphonuclear Leukocyte Transmigration In Vitro
Hypercontractile Female Hearts Exhibit Increased S-Nitrosylation of the L-Type Ca2+ Channel α1 Subunit and Reduced Ischemia/Reperfusion Injury
Accelerated Arteriosclerosis of Vein Grafts in Inducible NO Synthase−/− Mice Is Related to Decreased Endothelial Progenitor Cell Repair
Rotation of the Myocardial Wall of the Outflow Tract Is Implicated in the Normal Positioning of the Great Arteries
CD34−/CD133+/VEGFR-2+ Endothelial Progenitor Cell Subpopulation With Potent Vasoregenerative Capacities
FcγIIB and Cardiovascular Inflammatory Disease