Dr. Muhammad Imtiaz Ashraf

Stacks Image 2417

Dr. Muhammad Imtiaz Ashraf

Principal Investigator



Stacks Image 2402
Stacks Image 2419


Dr. Muhammad Imtiaz Ashraf did his PhD in 2012 in the laboratory of Prof. Jakob Troppmair, Dept. of Visceral-, Transplant- and Thoracic Surgery, Medical University of Innsbruck, Austria. In his doctoral thesis, he identified a novel and crucial role of p38MAPK in the regulation of ischemia reperfusion injury, in part, through its effects on mitochondrial functions. From 2012 to 2015, he was working in the same department as a post-doctoral scientist under supervision of Prof. Felix Aigner. There, he investigated the function role of Lcn2, an emerging biomarker of acute renal injury and graft rejection, in the course of renal allograft rejection. Since he moved to the department of surgery, Charite, Berlin in 2015, he has been involved in several projects aimed at elucidating critical mechanisms of renal allograft rejection and developing novel approaches for pre-transplant testing of solid organs. In particular, he teamed up with Prof. Felix Aigner and Prof Igor M. Sauer within CRC-Renoprotection (1365) on defining molecular and cellular mechanisms of rLcn2-mediated protection of the renal grafts. He has long-standing expertise in pre-clinical models of organ transplantation, including kidney and heart transplantation in the mouse and rat models.
His major current and future research interests aim at;

  1. Elucidating critical events responsible for physiological decline and high inflammatory properties of expanded criteria donor (ECD) organs, particularly kidneys. The ultimate objective is to overcome organ shortage through pre-implant reconditioning of ECD organs by targeting the candidate mechanisms using an EMP system.
  2. Identifying role of major structural components of an organ, namely epithelial cells, endothelial cells and fibroblasts in defining recipients’ immune response to that organ following transplantation. The ultimate objective is to devise novel organ specific therapeutic options, aimed at targeting the candidate mechanism in structural cells.

This website or its third-party tools use cookies, which are necessary to its functioning and required to achieve the purpose illustrated in the Disclaimer. By closing this banner, scrolling this page, clicking a link or continuing to browse otherwise, you agree to the use of cookies.