Jason Elinoff, M.D.


Pulmonary Vascular Biology Laboratory


Bldg. 10 CRC Room 3-5322 (office), Room 3-5288 (lab)
10 Center Drive
Bethesda, MD 20892
United States



Research Topics

Pulmonary arterial hypertension (PAH) is characterized by dysregulated cell proliferation and infiltration of activated inflammatory cells leading to progressive narrowing and obliteration of the distal pulmonary arteries. While current therapeutics reduce pulmonary arterial pressure and increase time to death or transplant, median survival remains only 5-7 years from diagnosis. Unlike selective pulmonary vasodilators alone, approaches directed at inflammatory vascular remodeling have the potential to arrest or even reverse the disease. The focus of the Pulmonary Vascular Biology Lab, led by Dr. Jason Elinoff, is the interplay between lung vascular endothelium and immune effector cells and their contributions to the development and progression of PAH. Current work includes in vitro profiling of human pulmonary artery endothelial cells with heterogeneous PAH-associated molecular defects in order to investigate molecular mechanisms that can exploited therapeutically. The overarching goal of the program is to translate basic science and pre-clinical studies to early phase therapeutic trials in PAH patients.


Dr. Elinoff earned his undergraduate degree in Chemistry from Princeton University and his degree in Medicine from the University of Chicago Pritzker School of Medicine. He went on to complete internship and residency training in Internal Medicine at the Massachusetts General Hospital. Dr. Elinoff completed his fellowship training in Critical Care Medicine at the NIH Clinical Center and Pulmonary and Critical Care Medicine at Johns Hopkins University.

Selected Publications

  1. Brusca SB, Elinoff JM, Zou Y, Jang MK, Kong H, Demirkale CY, Sun J, Seifuddin F, Pirooznia M, Valantine HA, Tanba C, Chaturvedi A, Graninger GM, Harper B, Chen LY, Cole J, Kanwar M, Benza RL, Preston IR, Agbor-Enoh S, Solomon MA. Plasma Cell-Free DNA Predicts Survival and Maps Specific Sources of Injury in Pulmonary Arterial Hypertension. Circulation. 2022;146(14):1033-1045.
  2. Lu M, Chen LY, Gairhe S, Mazer AJ, Anderson SA, Nelson JNH, Noguchi A, Siddique MAH, Dougherty EJ, Zou Y, Johnston KA, Yu ZX, Wang H, Wang S, Sun J, Solomon SB, Vanderpool RR, Solomon MA, Danner RL, Elinoff JM. Mineralocorticoid receptor antagonist treatment of established pulmonary arterial hypertension improves interventricular dependence in the SU5416-hypoxia rat model. Am J Physiol Lung Cell Mol Physiol. 2022;322(3):L315-L332.
  3. Gairhe S, Awad KS, Dougherty EJ, Ferreyra GA, Wang S, Yu ZX, Takeda K, Demirkale CY, Torabi-Parizi P, Austin ED, Elinoff JM, Danner RL. Type I interferon activation and endothelial dysfunction in caveolin-1 insufficiency-associated pulmonary arterial hypertension. Proc Natl Acad Sci U S A. 2021;118(11).
  4. Elinoff JM, Mazer AJ, Cai R, Lu M, Graninger G, Harper B, Ferreyra GA, Sun J, Solomon MA, Danner RL. Meta-analysis of blood genome-wide expression profiling studies in pulmonary arterial hypertension. Am J Physiol Lung Cell Mol Physiol. 2020;318(1):L98-L111.
  5. Elinoff JM, Chen LY, Dougherty EJ, Awad KS, Wang S, Biancotto A, Siddiqui AH, Weir NA, Cai R, Sun J, Preston IR, Solomon MA, Danner RL. Spironolactone-induced degradation of the TFIIH core complex XPB subunit suppresses NF-κB and AP-1 signalling. Cardiovasc Res. 2018;114(1):65-76.

Related Scientific Focus Areas

This page was last updated on Wednesday, July 10, 2024