Contact Info

OFFICE:  909 S Wolcott

              4143 COMRB

PH #:  (312) 355-0251


Glenn Marsboom, PhD


Research Interests

Pulmonary arterial hypertension (PAH) is characterized by structural remodeling and narrowing of pulmonary arteries. Such vascular remodeling increases the pulmonary vascular resistance and ultimately leads to right ventricular failure. The 5-year survival is currently only 66%, highlighting the importance of better understanding the underlying disease mechanisms to pave the way for targeted therapies. I’m currently focusing on the following two related projects:

1. Recently a novel frameshift mutation in Caveolin-1 (Cav1) was identified in a family with heritable PAH. This frameshift mutation leads to caveolin-1 protein that contains all known functional domains but has a change only in the final 20 amino acids of the C terminus. By using patient-derived fibroblasts, we hope to understand how this mutation leads to PAH.

2. While it has been known for 20 years that that mutations in BMPR2 are responsible for most cases of familial PAH, there are no specific treatments available for these patients. Using mice carrying a mutation found in hereditary PAH, we will study the activation state of fibroblasts and how these fibroblasts can promote pulmonary artery smooth muscle cell (PASMC) proliferation and amplify disease pathogenesis.

Selected Awards and Honors



Parker B. Francis Career Development Award

Scientist Development Grant, American Heart Association


Electron microscopy of fibroblasts derived from healthy controls (left panels) and patients with a c.474delA mutation in Caveolin-1 (right panels).

Lung sections from a wild type mouse & a MBPR2+/R899X

mouse were stained for the endothelial marker vWR (red)

and the smooth muscle cell marker aSMA(green).  A pronounced increase in vascular musclarization is observed in BMPR2+/

R899X mice, indicttating the development of PAH.

Selected Publications

Marsboom G, Chen Z, Yuan Y, et al. Aberrant Caveolin-1-Mediated Smad Signaling and Proliferation Identified by Analysis of Adenine 474 Deletion Mutation (c.474delA) in Patient Fibroblasts: A New Perspective in the Mechanism of Pulmonary Hypertension. Mol Bio Cell. 2017; 28(9):1177-1185.

Marsboom G, Zhang GF, Pohl-Avila N, et al. Glutamine Metabolism Regulates the Pluripotency Transcription Factor OCT4 in Human Embryonic Stem Cells. Cell Reports. 2016;16(2):323-32.

Marsboom G, Toth PT, Ryan JJ, et al. Dynamin-related protein 1-mediated mitochondrial mitotic fission permits hyperproliferation of vascular smooth muscle cells and offers a novel therapeutic target in pulmonary hypertension. Circulation Research. 2012;110(11):1484-97.

Marsboom G, Wietholt C, Haney CR, et al. Lung 18F-fluorodeoxyglucose PET for Diagnosis and Monitoring of Pulmonary Arterial Hypertension. Am J Respir Crit Care Medicine. 2012;185(6):670-9.

Marsboom G, Vermeersch P, Pokreisz P, et al. (2008). Sustained Endothelial Progenitor Cell Dysfunction after Chronic Hypoxia-Induced Pulmonary Hypertension. Stem Cells. 2008; 26(4):1017-26.

Marsboom G, Zhang M, Rehman J, Malik AB. Vascular repair and regeneration by endothelial progenitor cells. Lung Stem Cells in the Epithelium and Vasculature. 2015 (book chapter, ISBN 978-3-319-16231-7).

Marsboom G, Rehman J. Redox and metabolic regulation of transcription. Oncotarget. 2016; 7(49):80107-80108.