Dr Amin Ardestani

Biography	I completed my Bachelor's degree in Biology at Tarbiat Moalem University in 2004 in Tehran, Iran. I then pursued my master's thesis in Biochemistry at the Institute of Biochemistry and Biophysics (IBB) between 2005 and 2007 at the University of Tehran, Iran. Subsequently, I earned my PhD in Biology from the University of Bremen, Germany in 2013. From 2014 to 2023, I served as a senior researcher, and later as a junior group leader and principal investigator at the Islet Biology Laboratory at the Center for Biomolecular Interactions Bremen (CBIB), University of Bremen, Germany. Currently, I work as a Senior Lecturer in Metabolic Signaling at Biomedical Institute for Multimorbidity at Hull York Medical School (HYMS) at University of Hull.
Research Interests	My research primarily focuses on pancreatic islet biology, with a particular emphasis on signal transduction pathways in diabetes. My program specializes in identifying pathways leading to the death and loss of function in pancreatic β-cells, which causatively contribute to β-cell damage and severe diabetes progression. The central theme of my research is the selective targeting of complex intracellular signaling networks to either block β-cell death programs directly or enhance β-cell regenerative capabilities. This long-standing program has already led to the development of innovative treatment approaches for diabetes. Specifically, my research aims to identify the mechanisms of the Hippo and mTOR signaling pathways, which are master regulators of organ size, metabolism, regeneration, and tissue homeostasis in β-cells. I have been fortunate to secure several national and international grants and awards for my investigations into the molecular pathophysiology of the Hippo and mTOR signaling pathways, which are highly relevant in many diseases, including cancer, cardiovascular disease, and β-cell destruction in diabetes.
Scopus Author ID	16202172800
PhD Supervision Availability	Yes
PhD Topics	Most immediate research topics are to identify (1) the mechanisms of β-cell quiescence, vulnerability, and autoimmunity in type 1 diabetes and (2) exploit this mechanistic information to develop novel targets for β-cell repair and regeneration in type 1 diabetes.