Dr. Abdelali Agouni
Dr. Abdelali Agouni is an Associate Professor of Pharmacology and the coordinator of graduate studies at the College of Pharmacy, Qatar University. Dr. Agouni graduated with a BSc (Biochemistry) in 2003 and an MSc (Pharmacology) in 2005 from the University Louis Pasteur of Strasbourg (France) and a PhD in clinical and experimental Pharmacology from the University of Angers (France) in 2008. After graduating from his PhD, he joined in 2009 the University of Aberdeen (Scotland) as a post-doctoral research fellow at the School of Biological Sciences. In October 2011, he moved the University of Surrey as a tenured Assistant Professor of cardiovascular biology within the Faculty of Health and Medical Sciences. In 2015, he joined the college of Pharmacy of Qatar University as assistant professor of pharmacology and then in 2017 he was promoted to the rank of associate professor.
Dr. Agouni is an expert in cardiovascular and metabolic functions phenotyping (33 peer-reviewed publications to date and a h-index of 19 and a total number of citations of 1,587) and a strong experience in investigating intracellular signalling pathways using both cellular and transgenic animal models of obesity, diabetes and cardiovascular disease. The major focus of his research to date has been to gain a better understanding of the mechanisms linking obesity and diabetes to cardiovascular complications such as hypertension and atherosclerosis and develop new tools to prevent and reverse these co-morbidities. Dr. Agouni has an established expertise in inter-cellular communication and the role of circulating microvesicles as biomarkers and vectors of metabolic and cardiovascular dysfunctions. Dr. Agouni has expertise in collaborating on large clinical studies and currently contributes to a major clinical study on stroke with Hamad General Hospital (Qatar), a project recently funded by Qatar University and Qatar National Research Fund. Dr. Agouni has successfully managed several competitive research grants involving teams inside and outside of Qatar. He is currently senior investigator on multiple active grants with a cumulative research income of over $2 million in the past 4 years. Dr. Agouni has successfully supervised several undergraduate, MSc and PhD students.
Dr. Agouni’s expertise is recognized by the scientific community through invitations to the editorial boards of several journals. His expertise in metabolic and cardiovascular research fields is recognized both nationally and internationally and he regularly reviews major grant proposals for national and international funding bodies and agencies such as Medical Research Council UK, Diabetes UK, British Heart Foundation, Swiss Science Foundation, Dutch Heart Foundation, and the Dutch organization for health & healthcare innovation. In addition, he routinely acts as ad hoc reviewer for several international journals.
Dr. Agouni has a strong experience as educator and has a significant experience in both undergraduate and postgraduate teaching. His teaching quality is internationally recognised and in 2013 he achieved the status Fellow of the Higher Education Academy (FHEA).
The journey of Sestrin 2 in diabetes: From a biomarker of disease to a key effector in diabetic complications
In the past two decades, obesity has reached a global epidemic status affecting adults as well as pediatric populations. The high prevalence of obesity led to dramatic negative consequences on morbidity, mortality and quality of life in addition to a significant social and economic burden. The obesity epidemic is the result of a combination of effects which include genetic predisposition, increased intake of high-fat diets and decreased physical activity due to rapid urbanization and sedentary lifestyle. Obesity is associated with a high risk of type 2 diabetes predisposing patients to diabetic nephropathy, the leading cause of end-stage renal failure worldwide. Diabetic nephropathy is a major complication of diabetes, which affects about 30% to 40% of the patients with type 1 and type 2 diabetes, and ultimately leads to end-stage renal disease, which necessitates the need for routine dialysis or kidney transplant for patient survival. Thus, characterization of early biomarkers of diabetic nephropathy and development of therapeutic strategies that diminish the severity of diabetic nephropathy are very critical.
Sestrin 2 is a novel stress-induced protein which plays critical roles in the body defense against free radicals that are notorious to be increased in diabetes and cause damage to cells. Therefore, we have determined the role of Sestrin 2 in diabetes and evaluated its potential as an early biomarker for diabetes and diabetic nephropathy.
Our research found that the levels of Sestrin 2 in urine from diabetic patients were lower compared to healthy subjects and that these levels were even lower in diabetic patients with established diabetic nephropathy. Furthermore, low levels of Sestrin 2 were associated with increased levels of oxygen free radical, a characteristic feature of oxidative stress, a major contributor to kidney function damage. Using genetically modified mice where Sestrin 2 gene was deleted from birth (knock out mice), we have identified the significance of low Sestrin 2 levels on kidney function in diabetes. We observed that mice deficient for Sestrin 2 when fed a high fat diet to become obese or when injected with a chemical called “streptozotocin” to kill insulin-secreting beta cells in the pancreas to cause diabetes, developed a more severe nephropathy compared to mice that express Sestrin 2. Kidneys from obese and diabetic mice lacking Sestrin 2 had an excessive accumulation of fat and fibrotic tissue (becomes non-physiologically functional) in kidneys.
We provide here the first evidence that Sestrin 2 is a potential biomarker for the progression of kidney disease in diabetes and identified its renoprotective role in obesity and diabetes-induced nephropathy. Understanding the protective of Sestrin 2 should yield novel therapeutic interventions to effectively preserve kidney function in obesity and diabetes.