Dr. med. Christoph Schell
Pathology / Cell-Matrix Interaction / Fibrosis
Internal Senior Fellow
October 2021 - July 2022
CV
Current Position
Clinician-Scientist at the Institute of Surgical Pathology, Medical Center – University of Freiburg, Group Leader and
Academic training
2011 – 2014 PhD at SGBM graduate school, University of Freiburg
2002 – 2008 Medical School, LMU and TU Munich
Scientific Qualifications
2020 Habilitation in Experimental Pathology, University of Freiburg
(Mentor: Prof. Dr. M. Werner & Prof. Dr. T. Huber)
2014 Dissertation (Dr. rer. nat.), Faculty of Biology, University of Freiburg
(Supervisor: Prof. Dr. T. Huber)
2012 Dissertation (Dr. med.), LMU University of Munich
(Supervisor: Prof. Dr. A. Mayerhofer)
Postgraduate Positions
2017 – present Group Leader, Institute of Surgical Pathology, Medical Center - University of Freiburg
2016 – present Pathology Resident, Institute of Surgical Pathology, Medical Center - University of Freiburg
2014 – 2015 Junior Group Leader, Department of Nephrology, Medical Center - University of Freiburg
2011 – 2015 Research Fellow, Department of Nephrology, Medical Center - University of Freiburg
2010 – 2011 Internal Medicine Residency, Medical Center - University of Freiburg
2009 – 2010 Internal Medicine Residency, University Medical Center Regensburg
Miscellaneous (Honors, Awards)
2017 – 2020 Berta-Ottenstein Clinician Scientist Fellow
2014 Research Stipend – German Society of Nephrology
2013 – 2014 Clinician Scientist Fellowship – NAKSYS (EKFS)
Selected Publications
- Maier JI, Rogg M, Helmstädter M, Sammarco A, Schilling O, Sabass B, Miner JH, Dengjel J, Walz G, Werner M, Huber TB and Schell C. EPB41L5 controls podocyte extracellular matrix assembly by adhesome-dependent force transmission. Cell Reports. 2021 Mar 23;34(12):108883. doi: 10.1016/j.celrep.2021.108883.
- Rogg M, Maier JI, Dotzauer R, Artelt N, Kretz O, Helmstädter M, Abed A, Sammarco A, Sigle A, Sellung D, Dinse P, Reiche K, Yasuda-Yamahara M, Biniossek ML, Walz G, Werner M, Endlich N, Schilling O, Huber TB*, Schell C*. SRGAP1 Controls Small Rho GTPases To Regulate Podocyte Foot Process Maintenance. J Am Soc Nephrol. 2021 Jan 29:ASN.2020081126. doi: 10.1681/ASN.2020081126 - * shared senior authorship
- Schell C, Sabass B, Helmstaedter M, Geist F, Abed A, Yasuda-Yamahara M, Sigle A, Maier JI, Grahammer F, Siegerist F, Artelt N, Endlich N, Kerjaschki D, Arnold HH, Dengjel J, Rogg M, Huber TB. ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier. Dev Cell. 2018 Dec 17;47(6):741-757.
- Schell C*, Rogg M*, Suhm M*, Helmstädter M, Sellung D, Yasuda-Yamahara M, KretzO, Küttner V, Suleiman H, Kollipara L, Zahedi RP, Sickmann A, Eimer S, Shaw AS, Kramer-Zucker A, Hirano-Kobayashi M, Abe T, Aizawa S, Grahammer F, Hartleben B, Dengjel J, Huber TB. The FERM protein EPB41L5 regulates actomyosin contractility and focal adhesion formation to maintain the kidney filtration barrier. Proc Natl Acad Sci U S A. 2017 Jun 6;114(23):E4621-E4630. *contributed equally
- Brinkkoetter PT, Bork T, Salou S, Liang W, Mizi A, Özel C, Koehler S, Hagmann HH, Ising C, Kuczkowski A, Schnyder S, Abed A, Schermer B, Benzing T, Kretz O, Puelles VG, Lagies S, Schlimpert M, Kammerer B, Handschin C, Schell C, Huber TB. Anaerobic Glycolysis Maintains the Glomerular Filtration Barrier Independent of Mitochondrial Metabolism and Dynamics. Cell Rep. 2019 Apr 30;27(5):1551-1566.
FRIAS Research Project
MatrixCode: matrisome pathology
The “extracellular matrix” (ECM) encompasses all secreted, deposited, and soluble proteins in the interstitial milieu. In recent years, our perspective on ECM has changed on the functional and protein level, as we now understand the ECM less as a passive “scaffold”, and more as integral part of the diverse, complex, and dynamic signaling environment sustaining healthy tissue. By improved understanding of these complex aspects of the so-called “matrisome”, our opportunities to develop targeted therapies interacting with these processes in disease, scarring, and regeneration will be strengthened. The MatrixCode project aims to decipher how pathophysiological signaling depends on biochemical and biophysical modifications of the ECM. MatrixCode is compiled of four sub-projects focusing on different aspects of ECM signaling within wound healing and tumor biology. MatrixCode will strengthen ECM research in Freiburg by creating a critical mass of scientists, and strengthening ties to collaboration partners in Strasburg and worldwide. MatrixCode will lay the foundation for subsequent collaborative funding initiatives.