Recent Publications

• Epigenetic dysregulation of energy homeostasis drives aortic valve stenosis that is treatable with metformin

• Lymphatic System Development and Function

• Congenital Vascular and Lymphatic Diseases

• ADAM9 promotes type I interferon-mediated innate immunity during encephalomyocarditis virus infection

• Endothelial cell expression of a STING gain-of-function mutation initiates pulmonary lymphocytic infiltration

• Unveiling the Spatiotemporal Diversity of the Endothelium in Development: A Multi-Omics Approach

• Integrated Pathogenesis of Vascular and Cardiac Valve Disease

• Expression of a STING Gain-of-function Mutation in Endothelial Cells Initiates Lymphocytic Infiltration of the Lungs

• Chromatin Compaction in Noncompaction Cardiomyopathy

• Quantitative analysis of metabolic fluxes in brown fat and skeletal muscle during thermogenesis

• Lymphatic System in Organ Development, Function, and Regeneration

• Pathological MAPK activation-mediated lymphatic basement membrane disruption causes lymphangiectasia that is treatable with ravoxertinib

• Cation Channelopathies: Novel Insights into Generalized Lymphatic Dysplasia

• Human 3p14.3: A Regulatory Region in Transposition of the Great Arteries

• Response by Jung et al to Letter Regarding Article, "Sustained Activation of Endothelial YAP1 Causes Epithelioid Hemangioendothelioma"

• Extracardiac Progenitors: Moving Beyond the First and Second Heart Field

• Vascular and Lymphatic Malformations: Perspectives From Human and Vertebrate Studies

• Sustained Activation of Endothelial YAP1 Causes Epithelioid Hemangioendothelioma

• N-Acetyl Transferases: New Insights Into Human Congenital Cardiovascular Defects

• Super Enhancers: Enhancing Human Cardiogenesis

• KRAS or BRAF mutations cause hepatic vascular cavernomas treatable with MAP2K-MAPK1 inhibition

• Histone deacetylases 1 and 2 silence cryptic transcription to promote mitochondrial function during cardiogenesis

• The Adverse Vascular Effects of E-Cigarettes: Smoke Without the Fire

• Establishment and maintenance of blood-lymph separation

• TIP55, a splice isoform of the KAT5 acetyltransferase, is essential for developmental gene regulation and organogenesis

• RIP kinase 1-dependent endothelial necroptosis underlies systemic inflammatory response syndrome

• Hdac3 regulates lymphovenous and lymphatic valve formation

• Histone deacetylase 1 and 2 are essential for murine neural crest proliferation, pharyngeal arch development, and craniofacial morphogenesis

• Histone Deacetylase 3 Coordinates Deacetylase-independent Epigenetic Silencing of Transforming Growth Factor-β1 (TGF-β1) to Orchestrate Second Heart Field Development

• Plasticity of Hopx(+) type I alveolar cells to regenerate type II cells in the lung

• Targeted deletion of Tsc1 causes fatal cardiomyocyte hyperplasia independently of afterload

• Histone deacetylase 3 modulates Tbx5 activity to regulate early cardiogenesis

• Murine craniofacial development requires Hdac3-mediated repression of Msx gene expression

• Trichostatin A abrogates airway constriction, but not inflammation, in murine and human asthma models

• Histone deacetylase 3 regulates smooth muscle differentiation in neural crest cells and development of the cardiac outflow tract

• Highly efficient miRNA-mediated reprogramming of mouse and human somatic cells to pluripotency

• Acetylation of a conserved lysine residue in the ATP binding pocket of p38 augments its kinase activity during hypertrophy of cardiomyocytes

• Homeodomain only protein x is down-regulated in human heart failure

• Heart-healthy hypertrophy

• Hopx and Hdac2 interact to modulate Gata4 acetylation and embryonic cardiac myocyte proliferation

• Foxp1/2/4-NuRD interactions regulate gene expression and epithelial injury response in the lung via regulation of interleukin-6

• Inpp5f is a polyphosphoinositide phosphatase that regulates cardiac hypertrophic responsiveness

• Deletion of GSK-3beta in mice leads to hypertrophic cardiomyopathy secondary to cardiomyoblast hyperproliferation

• Transgenic overexpression of Hdac3 in the heart produces increased postnatal cardiac myocyte proliferation but does not induce hypertrophy

• Differential regulation of HOXA9 expression by nuclear factor kappa B (NF-kappaB) and HOXA9

• Homeobox gene HOXA9 inhibits nuclear factor-kappa B dependent activation of endothelium

• Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity