Patricio A. Leyton, MD
Department of Anesthesia, Critical Care and Pain Medicine
55 Fruit Street
Boston, MA 02144
Explore This Laboratory
Assistant in Research, Department of Anesthesia, Critical Care and Pain Medicine at Massachusetts General Hospital
- Mechanism by which mutations in the gene for the bone morphogenetic protein type 2 receptor lead to the development of Primary Pulmonary Arterial Hypertension
- New models to investigate vascular remodeling in the pulmonary circulation
- Pathogenesis of Pulmonary Hypertension
Description of Research
Our research aims to understand the mechanisms by which the mutation in a serine/threonine kinase receptor for bone morphogenetic proteins (BMPs), specifically the BMP type 2 receptor (BMPR2), participates in the development of Primary Pulmonary Arterial Hypertension (PAH). Among many functions, BMPs are known to be key regulators in vascular and lung development. Moreover, during adult life, BMPs are thought to maintain the vasculature integrity of the lung. Elucidating how mutations in BMPR2 lead to PAH will help us to find new therapeutical approaches to treat this life-threatening condition.
Medoff BD, Okamoto Y, Leyton P, Weng M, Sandall BP, Raher MJ, Kihara S, Bloch KD, Libby P, Luster AD. Adiponectin deficiency increases allergic airway inflammation and pulmonary vascular remodeling. Am J Respir Cell Mol Biol. 2009 Oct;41(4):397-406. Epub 2009 Jan 23.
Weng M, Raher MJ, Leyton P, Combs TP, Scherer PE, Bloch KD, Medoff BD. Adiponectin Decreases Pulmonary Arterial Remodeling in Mouse Models of Pulmonary Hypertension. Am J Respir Cell Mol Biol. 2011 Aug;45(2):340-7. Epub 2010 Nov 12.
Steinbicker AU, Bartnikas TB, Lohmeyer LK, Leyton P, Mayeur C, Kao SM, Pappas AE, Peterson RT, Bloch DB, Yu PB, Fleming MD, Bloch KD. Perturbation of hepcidin expression by BMP type I receptor deletion induces iron overload in mice. Blood. 2011 Oct 13;118(15):4224-30. Epub 2011 Aug 12.