Prof. Walter Wahli (PhD)

Professor of Metabolic Disease in Lee Kong Chian School of Medicine, Nanyang Technological University & Imperial College London

Founder of the Center for Intergrative genomics, Lausanne



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Walter Wahli is Professor of Metabolic Disease in Lee Kong Chian School of Medicine, Nanyang Technological University & Imperial College London. Prior to this appointment, Prof Wahli spent most of his scientific career at the world-renowned University of Lausanne, Switzerland. He obtained his PhD in 1977 under the guidance of Prof. Weber at the University of Berne.

He was appointed Full Professor and Director of the Institute of Animal Biology of the University of Lausanne in 1980. He is also the Founder Director of the Center for Integrative Genomics at Lausanne. He has been postdoctoral fellow at the Department of Embryology, Carnegie Institution of Washington in Baltimore, USA, and Visiting associate at the National Institutes of Health (NIH), Bethesda, USA.

He has published more than 300 papers in top-ranking journals, book chapters and editorials. He was awarded several prizes and recently received the Lifetime Achievement Award from the Faculty of Biology and Medicine, University of Lausanne.

  • Energy metabolism 90%
  • PPARs 86%
  • Fatty acids and eicosanoids 51%


Our main research efforts are focused on control of epithelial tissue homeostasis and carcinogenesis, using skin as model system. We are focusing on two key questions:

1) the intracellular regulatory mechanisms that control the balance between squamous cell differentiation and tumorgenesis;

2) the role of mesenchymal stromal cells in control of tissu aging, inflammation and keratinocyte tumor development.

Currently, Prof. Dotto is the principle investigator of a major ICPI-supported development initiative on cervical cancer prevention in Cameroon. This project aims to invest in the sustainable development of the local public health care system while extracting valuable epidemiological data and novel molecular science.


  1. C. Dreyer*, G. Krey*, H. Keller, F. Givel, G. Helfenbein and W. Wahli (1992). Control of the peroxisomal β-oxidation pathway by a novel family of nuclear hormone receptors. Cell, 68, 879-887. * Co-first authors.
  2. P.R. Devchand, H. Keller, J.M. Peters, M. Vazquez, F.J. Gonzalez and W. Wahli (1996). The PPARb – leukotriene B4 pathway to inflammation control. Nature 384, 39-43.
  3. S. Kersten, J. Seydoux, J.M.Peters, F.J. Gonzalez, B. Desvergne and W, Wahli (1999). Peroxisome proliferator-activated receptor alpha mediates the adaptive response to fasting. Journal of Clinical Investigation 103, 1489-1498.
  4. S. Kersten, B. Desvergne and W. Wahli (2000). Roles of PPARs in health and disease. Nature, 405, 421-424.
  5. L. Michalik, B. Desvergne, S. Basu-Modak, P. Escher, J.M. Peters, G. Kaya, F.J. Gonzalez J. Zakany, D. Metzger, P. Chambon, D. Duboule and W. Wahli (2001). Impaired skin wound healing in peroxisome proliferator-activated receptor (PPAR)b and PPARd mutant mice. The Journal of Cell Biology, 154, 799-814.
  6. N.S. Tan, L. Michalik, N. Noy, R. Yasmin, C. Pacot, M. Heim, B. Flühmann, B. Desvergne and W. Wahli (2001). The critical roles of PPARβ in cellular response to inflammation. Genes & Development, 15, 3263-3277.
  7. N. Di-Poï, N.S. Tan, L. Michalik, W. Wahli and B. Desvergne (2002). Anti-apoptotic role of PPARβ in keratinocytes via transcriptional control of the Akt1 signaling pathway. Molecular Cell, 10, 721-733.
  8. L. Michalik, B. Desvergne, W. Wahli (2004). Peroxisome-Proliferator-Activated Receptors and Cancers : Complex Stories. Nature Reviews Cancer, 4, 61-70.
  9. M. Schuler, F. Ali, C. Chambon, D. Duteil, J-M. Bornet, A. Tardivel, B. Desvergne, W. Wahli, P. Chambon, D. Metzger (2006). PGC1alpha expression is controlled in skeletal muscles by PPARβ, whose ablation results in fiber type switching, obesity and type 2 diabetes. Cell Metabolism, 4, 407-414.
  10. Leuenberger, S. Pradervand and W. Wahli (2009) Sumoylated PPARα mediates gender-specific gene repression and protects the liver from estrogen-induced toxicity. Journal of Clinical Investigation 119, 3138–3148.