van Rooij group
Eva van Rooij
Eva van Rooij attended University Hospital Maastricht in the Netherlands where she received a Ph.D. at the department of Cardiology. She then went on to complete postdoctoral training in Molecular Biology at UT Southwestern Medical Center in the lab of Dr. Eric Olson where she served as lead scientist in the studies that linked microRNAs to cardiovascular disease. Her work subsequently became the foundation of miRagen Therapeutics, Inc., a company focused on the development of microRNA therapeutics, where she functioned as head of research till 2012 and current still serves as special advisor and scientific advisory board member.
In 2013 she started an academic lab at the Hubrecht Institute to further unveil the molecular signaling pathways that are relevant for cardiac biology. In 2013, she was awarded a prestigious ERC consolidator grant to study the function of microRNA in heart and metabolic disease. In 2014 she was a co-recipient of a transatlantic Fondation Leducq Network grant to dissect mechanism to enhance cardiac regeneration and she received the Outstanding Achievement Award for 2014 from the European Society of Cardiology council on Basic Cardiovascular Science. In her current work she combines mouse genetics, the use of animal models of heart disease, animal physiology and molecular biology to identify the important pathways for cardiac remodeling and repair.
- Professor at Utrecht University
- Advisor at miRagen Therapeutics (paid)
Team members van Rooij
Brian van Kampen
Hesther de Ruiter
Monika Gladka-de Vries
Anne Katrine Johansen
Mariska van Geldorp
Eva van Rooij
A major challenge in the field of cardiac biology is to decipher the relevance of different signaling mechanisms during disease. Our lab aims to unravel the molecular pathways that underlie heart disease by studying the complex interplay between gene expression and microRNAs. While the heart is notoriously resistant to repair, considerable evidence suggests that the fundamental biology of the myocardium provides multiple opportunities to stimulate or boost these endogenously present repair mechanisms, with the ultimate aim to enhance cardiac regeneration to maintain a better cardiac output. Using molecular in vitro and in vivo gain and loss-of-function studies, applying both...
Montgomery RL, Yu G, Latimer PA, Stack C, Robinson K, Dalby CM, Kaminski N, van Rooij E. MicroRNA mimicry blocks pulmonary fibrosis. EMBO Mol Med (2014). [pdf]
Hullinger TG, Montgomery RL, Seto AG, Dickinson BA, Semus HM, Lynch JM, Dalby CM, Robinson K, Stack C, Latimer PA, Hare JM, Olson EN, van Rooij E. Inhibition of miR-15 protects against cardiac ischemic injury. Circ Res (2012) 6;110(1): 71-81. [pdf]
Montgomery RL, Hullinger TG, Semus HM, Dickinson BA, Seto AG, Lynch JM, Stack C, Latimer PA, Olson EN, van Rooij E. Therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure. Circulation (2011) 4;124(14): 1537-1547. [pdf]
van Rooij E, Sutherland LB, Thatcher JE, DiMaio JM, Naseem RH, Marshall WS, Hill JA, Olson EN. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. Proc Natl Acad Sci U S A. (2008) 105(35): 13027-13032. [pdf]
van Rooij E, Sutherland LB, Qi X, Richardson JA, Hill J, Olson EN. Control of stress-dependent cardiac growth and gene expression by a microRNA. Science (2007) 27; 316(5824): 575-579. [pdf]