We make use of an inducible cardiomyocyte-specific promoter crossed to R26 Confetti to allow us to study cardiomyocytes proliferation within the heart
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The Van Rooij group aims to delineate signaling pathways relevant for heart repair and remodeling that can eventually lead to effective treatment options to minimize the loss of cardiomyocytes and/or reverse the adverse remodeling processes in the diseased heart.
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.
Specific areas of focus in our lab are:
In response to stress the heart undergoes a remodeling response to cope with the increase in workload. Under conditions of physiological stress, like exercise, the heart shows a reversible, beneficial remodeling response, during which the heart muscle cells (cardiomyocytes) enlarge while the cardiac function remains preserved. However, under pathological conditions, such as myocardial infarction or hypertension, the heart exerts a maladaptive, pathological remodeling response, which is detrimental for cardiac function.
Our lab makes use of animal models of either physiological or pathological remodeling to study the underlying molecular pathways of these remodeling responses. Improving our understanding of the factors involved in these processes might aid us in developing new and better therapies.
Cardiac injury induces the loss of viable heart muscle cells, cardiomyocytes. 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 repair mechanisms. Our lab is focused on enhancing these endogenously present repair mechanisms as well as defining new ways to restore more viable tissue after damage. We do this by studying new cells types in the heart that can contribute to the generation of new myocytes and by defining the mechanisms that can trigger cardiomyocyte division upon damage. Identification of new factors, genes or epigenetic regulators involved in heart repair might ultimately aid to improve cardiac integrity upon damage to maintain a better cardiac function after an infarct.
While novel treatment opportunities for heart disease, like microRNA therapeutics, are often effective, systemic delivery induces a low cardiac exposure and can lead to undesirable effects in other tissues. For this reason, our lab aims to explore localized delivery options to increase cardiac delivery while preventing unwanted side effects. We do this through the identification of novel cardiac-restricted receptors to serve as drug-conjugates. Additionally, we explore the use of delivery vehicles, such as hydrogels and buffers, to enhance delivery of therapies to the heart.
Many types of heart disease are caused by a genetic disorder. While many of these diseases are caused by a specific mutation, often very little is known about the molecular pathways that are responsible for the remodeling responses that characterize the disease. Our lab uses both cardiomyoctes derived from human stem cells (iPS cell-derived cardiomyocytes) and mouse models harboring the human mutation to study which exact changes occur during the onset and development of the disease. By doing so we aim to contribute to the development of improved treatment options for patients suffering from this disease.
Tsui H, van Kampen SJ, Han SJ, Meraviglia V, van Ham WB, Casini S, van der Kraak P, Vink A, Yin X, Mayr M, Bossu A, Marchal GA, Monshouwer-Kloots J, Eding J, Versteeg D, de Ruiter H, Bezstarosti K, Groeneweg J, Klaasen SJ, van Laake LW, Demmers JAA, Kops GJPL, Mummery CL, van Veen TAB, Remme CA, Bellin M, van Rooij E.
Monika M Gladka, Arwa Kohela, Bas Molenaar, Danielle Versteeg, Lieneke Kooijman, Jantine Monshouwer-Kloots, Veerle Kremer, Harmjan R Vos, Manon M H Huibers, Jody J Haigh, Danny Huylebroeck, Reinier A Boon, Mauro Giacca, Eva van Rooij
Arwa Kohela, Sebastiaan J. van Kampen, Tara Moens, Martijn Wehrens, Bas Molenaar, Cornelis J. Boogerd, Jantine Monshouwer-Kloots, Ilaria Perini, Marie José Goumans, Anke M. Smits, J. Peter van Tintelen, and Eva van Rooij.
Wehrens M, de Leeuw AE, Wright-Clark M, Eding JEC, Boogerd CJ, Molenaar B, van der Kraak PH, Kuster DWD, van der Velden J, Michels M, Vink A, van Rooij E.
van Kampen SJ, Han SJ, van Ham WB, Kyriakopoulou E, Stouthart EW, Goversen B, Monshouwer-Kloots J, Perini I, de Ruiter H, van der Kraak P, Vink A, van Laake LW, Groeneweg JA, de Boer TP, Tsui H, Boogerd CJ, van Veen TAB, van Rooij E
Monika M Gladka, Anne Katrine Z Johansen, Sebastiaan J van Kampen, Marijn M C Peters, Bas Molenaar, Danielle Versteeg, Lieneke Kooijman, Lorena Zentilin, Mauro Giacca, Eva van Rooij
Boogerd CJ, Lacraz GPA 1, Vértesy A, van Kampen SJ, Perini I, de Ruiter H, Versteeg D, Brodehl A, van der Kraak PH, Giacca M, de Jonge N, Junker JP, van Oudenaarden A, Vink A, van Rooij E.
Molenaar B, Timmer LT, Droog M, Perini I, Versteeg D, Kooijman L, Monshouwer-Kloots J, de Ruiter H, Gladka MM, van Rooij E
Gladka MM, Molenaar B, de Ruiter H, Versteeg D, Lacraz GPA, van der Elst S, Huibers MMH, van Oudenaarden A, van Rooij E.
Lacraz GPA, Junker JP, Gladka MM, Molenaar B, Scholman KT, Vigil-Garcia M, Versteeg D, de Ruiter H, Vermunt MW, Creyghton MP, Huibers MMH, de Jonge N, van Oudenaarden A, van Rooij E.
Johansen AK, Molenaar B, Versteeg D, Leitoguinho AR, Demkes CJ, Spanjaard B, de Ruiter H, Akbari Moqadam FA, Kooijman L, Zentilin L, Giacca M, van Rooij E.
van Rooij E, Sutherland LB, Qi X, Richardson JA, Hill J, Olson EN.
Marta Vigil-Garcia, Charlotte J Demkes, Joep E C Eding, Danielle Versteeg, Hesther de Ruiter, Ilaria Perini, Lieneke Kooijman, Monika M Gladka, Folkert W Asselbergs, Aryan Vink, Magdalena Harakalova, Alexander Bossu, Toon A B van Veen, Cornelis J Boogerd, Eva van Rooij
Kohela A, van Rooij E.
Timmer LT, van Rooij E.
van Kampen SJ, van Rooij E.
Sebastiaan Johannes van Kampen, Eva van Rooij
Eding JEC, van Rooij E.
Molenaar B, van Rooij E.
Eding JE, Demkes CJ, Lynch JM, Seto AG, Montgomery RL, Semus HM, Jackson AL, Isabelle M, Chimenti S, van Rooij E.
Van Rooij E.
Montgomery RL, Yu G, Latimer PA, Stack C, Robinson K, Dalby CM, Kaminski N, van Rooij E
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.
Montgomery RL, Hullinger TG, Semus HM, Dickinson BA, Seto AG, Lynch JM, Stack C, Latimer PA, Olson EN, van Rooij E.
Eva van Rooij is group leader at the Hubrecht Institute and professor of Molecular Cardiology at the University Medical Center Utrecht. Her group aims to unveil the molecular signaling pathways that are relevant for cardiac disease. The Van Rooij group combines mouse genetics and models of heart disease with novel sequencing technologies such as single-cell sequencing and Tomo-seq to identify key cell types or candidate factors important for specific remodeling and repair processes of the heart. The ultimate goal is to identify pathways that can eventually lead to effective treatment options to minimize the loss of cardiomyocytes and/or reverse the adverse remodeling processes in the diseased heart.
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Anne Katherine Johansen
Monika Gladka-de Vries
Maya Wright Clark
Anne de Leeuw
Sebastiaan van Kampen