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 her complete postdoctoral training in Molecular Biology at UT Southwestern Medical Center in the lab of Dr. Eric Olson where she served as a 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. Additionally, she still serves as a special advisor and scientific advisory board member.
Currently, she runs an academic lab at the Hubrecht Institute to further unveil the molecular signaling pathways that are relevant for cardiac disease. In 2013, she was awarded a prestigious ERC consolidator grant to study the function of microRNAs in heart and metabolic diseases. In 2014 she was a co-recipient of a transatlantic Fondation Leducq Network grant to dissect mechanisms to enhance cardiac regeneration. In 2014, she received the Outstanding Achievement Award from the European Society of Cardiology council on Basic Cardiovascular Science. In 2015 she received a CVON grant from the Dutch Heart foundation and a grant from the Dutch Life Sciences & Health sector and was appointed Professor in Molecular Cardiology at the Dept. of Cardiology at the UMCU. In 2016 she was a recipient of a European network grant (ERA-CVD) focussed on heart repair after ischemic damage. In 2017 she received the Ammodo-KNAW award for ourstanding fundamental research.
In her current work she combines mouse genetics and models of heart disease with state-of-the-art sequencing technologies (such as single-cell sequencing and tomo-seq) and high-end molecular biology techniques to identify the important pathways for cardiac remodeling and repair and to explore ways to enhance cardiac efficacy of new drugs.
• Professor at Dept. of Cardiology, University Medical Center Utrecht
• Special advisor and scientific advisory board member miRagen Therapeutics (paid)
• Associated editor JACC BTR (paid)
Team members van Rooij
Monika Gladka-de Vries
Anne Katrine Johansen
Brian van Kampen
Eva van Rooij
Hesther de Ruiter
Kees Jan Boogerd
A major challenge in the field of cardiac biology is to decipher the relevance of different signaling mechanisms that are relevant during disease. Using mouse genetics in combination with novel sequencing technologies our lab is able to identify key cell types or candidate factors important for specific remodeling and repair processes of the heart. These factors are studied in detail by molecular gain and loss-of-function studies, applying both genetics and oligonucleotide-based approaches. The van Rooij lab aims to delineate signaling pathways relevant for heart repair and remodeling that can eventually lead to effective treatment options to minimize the loss...
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]