Short CV/Education and training

  • 1992 – 1997
    Studied pharmacy at the University of Vienna, Austria

  • 1997
    Completed study course as a Magistra Pharmacia; Diplom degree in clinical pharmacy, grade: excellent, University of Vienna, Austria

  • 1998
    Licenced as a pharmacist in Hannover, Germany

  • 1998 – 1999
    Pharmacist in Hannover, specialisation: clinical pharmacy, geriatrics and diabetes

    Instructor of pharmacology, pathophysiology and pharmaceutical practice in Bückeburg, Germany

  • 1999
    Certified course in clinical pharmacy in London, UK, School of Pharmacy; University of Tübingen, Germany; Ulm University Hospital, Germany

  • 2000 – 2003
    PhD at University Hospital of Zurich, Switzerland

  • 2002 – 2004
    Project director in the Division of Endocrinology and Diabetes, University Hospital of Zurich

  • Since 2005
    Associate member of the Molecular Biology Institute, UCLA, USA

  • 2005 – 2008
    Assistant professor at the Larry Hillblom Islet Research Centre, University of California (UCLA), Los Angeles, CA, USA

  • Since 2008
    Director of the Islet Biology Laboratory, Centre for Biomolecular Interactions, University of Bremen, Germany

Selected publications

  • Maedler, K. et al., FLIP switches Fas-mediated glucose signaling in human pancreatic β-cells from apoptosis to cell replication. Proc.Natl.Acad.Sci.U.S.A 99:8236-8241, 2002

  • Maedler, K et al., Glucose-induced beta-cell production of interleukin-1beta contributes to glucotoxicity in human pancreatic islets. J.Clin.Invest 110:851-860, 2002

  • Mädler, K. et al.: Low concentration of IL-1-beta induces FLIP-mediated – cell proliferation in human pancreatic islets. In: Diabetes 55, 2006. S. 2713-2722.

  • Mädler, K. et al.: Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases. In: FASEB J. 22(6), 2008. S. 1905-1913.

  • Maedler,K et al., Leptin modulates β cell expression of IL-1 receptor antagonist and release of IL-1β and in human islets. Proc.Natl.Acad.Sci.U.S.A 101: 8138-43, 2004

  • Shu, L. et al.: Transcription factor 7-like 2 regulates beta-cell survival and function in human pancreatic islets. In: Diabetes 57(3), 2008. S. 645-653.

  • Sauter, N.S. et al.: The antiinflammatory cytokine interleukin-1 receptor antagonist protects from high-fat diet-induced hyperglycemia. In: Endocrinology 149(5), 2008. S. 2208-2218.

  • Schulthess, F.T. et al.: CXCL10 impairs beta cell function and viability in diabetes through TLR4 signaling. In: Cell Metab. 9(2), 2009. S. 125-139.

  • Shu, L. et al.: Decreased TCF7L2 protein levels in T2DM correlate with downregulation of GIP- and GLP-1 receptors and impaired beta-cell function. In: Hum Mol Gen 18(13), 2009. S. 2388-2399.

  • Owyang A*, Maedler K* et al.: XOMA 052, an Anti-IL-1 beta Monoclonal Antibody, Improves Glucose Control and Beta Cell Function in the Diet-Induced Obesity Mouse Model, Endocrinology. 2010;151(6):2515-27

  • Oetjen, J et al., Benchmark datasets for 3D MALDI- and DESI-imaging mass spectrometry, GigaScience (2015) 4:20

  • Ardestani, A et al., MST1 is a key regulator of beta cell apoptosis and dysfunction in diabetes. Nature Medicine, 2014 VOLUME 20 , NUMBER 4 , APRIL 2014

Complete list of publications


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  1. Decoding Diabetes

    Prof. Kathrin Maedler and her colleagues have found a key protein underlying the loss of insulin-producing pancreatic beta cells. Therapeutic strategies targeting this protein could protect beta cells both in type 1 and in type 2 diabetes.