Rik Lories

 

Rik Lories (KU Leuven), MD, PhD, Professor of Rheumatology, Skeletal Biology and Engineering Research Center

 

 

Rik Lories directs the Laboratory for Tissue Homeostasis and Disease that is part of the Skeletal Biology and Engineering Research Center at KU Leuven. He is a consultant physician in the Division of Rheumatology at the University Hospitals Leuven. KU Leuven, the largest and oldest university in Belgium, ranks 49th in the Times Higher Education World 2019 Ranking and tops Reuter’s 2019 ranking of Europe’s most innovative universities.


His research focuses on endogenous tissue responses in the joint with specific attention towards translational questions in chronic arthritis, in particular osteoarthritis, axial spondyloarthritis, and psoriatic arthritis. Currently full Professor (“gewoon hoogleraar”) at KU Leuven, he obtained his medical degree summa cum laude in 1996. He subsequently started specialty training in internal medicine and rheumatology. In 2003, he was certified as rheumatologist. In 2003 he also obtained a PhD in biomedical sciences at KU Leuven. He received PhD (4 years) and Postdoctoral fellowships (6 years) from the Flanders Research Foundation.

As past chair of the EULAR (European League against Rheumatism) Standing Committee on investigative rheumatology, he was a member of EULAR’s Executive Committee from 2014 to 2017. Currently, he serves as associate editor for the journals Osteoarthritis and Cartilage, RMD Open and Rheumatology (2014-2017). He has (co-)authored 159 publications, including original research reports or reviews in Nature Medicine, Science Translational Medicine, Nature Communications, Journal of Clinical Investigation, PNAS, Nature Reviews Rheumatology, Osteoarthritis and Cartilage, Annals of the Rheumatic Diseases and Arthritis and Rheumatology

Recent key research papers:

  • Cornelis F., Monteagudo S., Guns L-A., Den Hollander W., Nelissen R., Storms L., Peeters T., Jonkers I., Meulenbelt I., Lories R (2018). ANP32A regulates ATM expression and prevents oxidative stress in cartilage, brain and bone. Science Translational Medicine, 10 (458)
  • Monteagudo, S., Cornelis, F., Aznar-Lopez, C., Yibmantasiri, P., Guns, L.A., Carmeliet, , Cailotto, F., Lories, R (2017). DOT1L safeguards cartilage homeostasis and protects against osteoarthritis. Nature  Communications, 19 (8): 15889. doi:10.1038/ncomms15889.
  • Bomer, N., Cornelis, F., Ramos, Y., den Hollander, W., Storms, L., van der Breggen, R., Lakenberg, N., Slagboom, P., Meulenbelt, I., Lories, R. (2016). The effect of forced exercise on knee joints in Dio2-/- mice: type II iodothyronine deiodinase-deficient mice are less prone to develop OA-like cartilage damage upon excessive mechanical stress, Annals of the Rheumatic Diseases, 75 (3), 571-7.
  • Castaño Betancourt, M., Cailotto, F., Kerkhof, H., Cornelis, F., Doherty, S., Hart, D., Hofman, A., Luyten, F., Maciewicz, R., Mangino, M., Metrustry, S., Muir, K., Peters, M., Rivadeneira, F., Wheeler, M., Zhang, W., Arden, N., Spector, T., Uitterlinden, A., Doherty, M., Lories, R., Valdes, A., van Meurs, J. (2012). Genome-wide association and functional studies identify the DOT1L gene to be involved in cartilage thickness and hip osteoarthritis, Proceedings of the National Academy of Sciences of the United States of America, 109 (21), 8218-8223. (shared last authorship).
  • Lories, R., Derese, I., Luyten, F. (2005). Modulation of bone morphogenetic protein signaling inhibits the onset and progression of ankylosing enthesitis, Journal of Clinical Investigation, 115 (6), 1571-1579.

Print