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You are here: FRIAS Fellows Fellows 2021/22 Dr. med. Christoph Schell

Dr. med. Christoph Schell

University Medical Center Freiburg
Pathology / Cell-Matrix Interaction / Fibrosis

Internal Senior Fellow
October 2021 - July 2022

Room 01 026
Phone +49 (0)761 - 270 80650
Fax +49 (0)761 203 97451


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.