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You are here: FRIAS Fellows Fellows 2016/17 Prof. Dr. Ketan Patel

Prof. Dr. Ketan Patel

University of Reading
Developmental Biology and tissue regeneration
External Senior Fellow
August 2015 - July 2016

Room 01 027
Phone +49 (0) 761-203 97440
Fax 49 (0) 761-203 97451


1988 PhD, Imperial College London.
1993 - 1996 MRC Postdoctoral Fellow, National Institute for Medical Research, Mill Hill, UK.
1996 - 1998
Wellcome Trust Research Fellow, University College London, London, UK.
1998 – 2001 Lecturer, University of Reading, UK.
2001 – 2007 Professor of Developmental Biology, Royal Veterinary College, London, UK.
2007 – Present Professor of Developmental Biology, University of Reading, UK.
2010- Present Molecular and physiopathological basis of Muscular Dystrophies Commission, The French Muscular Dystrophy Association (AFM).
2010- Present Member of the Genes and Development and Science Technology Engineering and Maths approaches to Biology board of the Biotechnology and Biological Sciences Research Council (BBSRC).
2013 – Present Editorial board, Nature Scientific Reports, American Journal of Stem cells, Editorial board, International Journal of Sports and Exercise Medicine.


Selected Publications

  • Symmorphosis through Dietary Regulation: A Combinatorial Role for Proteolysis, Autophagy and Protein Synthesis in Normalising Muscle Metabolism and Function of Hypertrophic Mice after Acute Starvation. Collins-Hooper H, Sartori R, Giallourou N, Matsakas A, Mitchell R, Makarenkova HP, Flasskamp H, Macharia R, Ray S, Swann JR, Sandri M, Patel K. PLoS One. (2015) 10(5):e0128731
  • Propeptide mediated inhibition of myostatin increases muscle mass through inhibiting proteolytic pathways in aged mice. Collins-HooperH, Matsakas A, Foster K, Dash PD Sartori R, Macharia R, Sandri M, Patel K, Journal of Gerontology (2014) 69:1049-59
  • Myostatin is a key mediator between energy metabolism and endurance capacity of skeletal muscle. Mouisel E, Relizani K, Mille-Hamard L, Denis R, Hourdé C, Agbulut O, Patel K, Arandel L, Morales-Gonzalez S, Vignaud A, Garcia L, Ferry A, Luquet S, Billat V, Ventura-Clapier R, Schuelke M, Amthor H.Am J Physiol Regul Integr Comp Physiol. (2014) 15:R444-54.
  • Blockade of ActRIIB signaling triggers muscle fatigability and metabolic myopathy. Relizani K, Mouisel E, Giannesini B, Hourdé C, Patel K, Morales Gonzalez S, Jülich K, Vignaud A, Piétri-Rouxel F, Fortin D, Garcia L, Blot S, Ritvos O, Bendahan D, Ferry A, Ventura-Clapier R, Schuelke M, Amthor H.Mol Ther. (2014) 22:1423-33.
  • Discovery of a mammalian splice variant of myostatin that stimulates myogenesis. Jeanplong F, Falconer SJ, Oldham JM, Thomas M, Gray TS, Hennebry A, Matthews KG, Kemp FC, Patel K, Berry C, Nicholas G, McMahon CD. PLoS One. (2013) 8:e81713.


FRIAS Research Project

Connectivity Map - A transcriptional approach for drug repurposing and its application to kidney disease and the ageing kidney


A central aim of this proposal is to identify FDA-approved molecules that can attenuate the degeneration of tissues associated with kidney diseases. The scope of our work focuses not only on the differing cells types that affect renal function in kidney diseases but also those associated with this pathology especially the skeletal muscle. This holistic approach allows us to examine and eventually treat the entire pathological landscape involved in kidney disease.

The work packages envisaged for this programme all map strategically on to the goals of the FRIAS Research Focus plan for the academic year 2015/16. We aim to isolate by FACS individual cell type from young and aged kidney as well as individual cells types from diseased (Diabetic model) and health kidney and generate C-Map for each population. Thereafter feed into the bio-informative pipeline to identify putative FDA approved compounds capable to alleviating the age and disease related changes in kidney cells. In addition, we will determine the mechanism of skeletal muscle loss, especially the role of autophagy in a model of acute kidney disease and the benefits to whole animal function of strategies that maintain muscle mass through antagonism of myostatin based signaling. Furthermore, use these experiments to feed into the C-Map pipeline to identify compounds capable to preventing acute kidney induced muscle atrophy.