Carmen Hurtado del Pozo

The driving theme of Dr. Carmen Hurtado’s academic career has been the understanding of molecular and genetic mechanisms of obesity and diabetes. Towards this goal, Carmen studied Biological Sciences as an undergraduate at the Complutense University in Madrid, Spain. In 2006, Carmen received a Fellowship from Spanish National Research Council (CSIC), with which she undertook a PhD in Biology with Professor Maria Jesus Obregon Perea, expert in brown adipose tissue, at Instituto de Investigacion Biomédica CSIC. The training during her PhD involved bench-side research training and coursework in metabolism, and molecular biology with direct application to the mechanisms of obesity in adipocytes. As a product of this work, Carmen published three articles as a first author in International Journals in first quartile and other two articles with important collaborators in the field of Obesity. Her Ph.D. was awarded cum laude in July 2011. In December 2011 Carmen joined the laboratory of Professor Ann Marie Schmidt with appointment at New York University in Diabetes Research Program, Division of Endocrinology. In 2014 she received a postdoctoral fellowship from the American Diabetes Association (ADA). Since then Carmen worked on projects investigating the role of Receptor for Advanced Glycation End products (RAGE) in obesity. In these four years, she published a co-first author paper in Diabetes (Rage regulates the metabolic and inflammatory response to high-fat feeding in mice) and several reviews with Professor Ann Marie Schmidt. Her main project has been submitted recently and it is now under revision in a high impact factor journal.

Group: Pluripotent stem cells and activation of endogenous tissue programs for organ regeneration
Supervisor: Núria Montserrat
Project: Developing regenerative strategies for kidney healing

Diabetes mellitus (DM) is one of the main threats to public health in developed countries. One of the most common detrimental complications is Diabetic Nephropathy (DN). DN is a syndrome of albuminuria, declining glomerular filtration rate (GFR), arterial hypertension, and increased cardiovascular risk that affects 25%-40% of type 1 (insulin dependent) and type 2 (non-insulin dependent) diabetic patients (DMT2). DN is the leading cause of end-stage renal disease, present in approximately 25%-40% of patients with long-standing Diabetes worldwide. To date, clinical interventions in the treatment of DN are very limited, and none of them can stop the development of DN. There is an urgent need for a regenerative strategy and induced pluripotent stem cells (iPSC) have shown potential as a therapeutic strategy. The main goal of this proposal is to develop 3 dimensional renal-derived structures as a model to study DN. To this end, we will generate GFP reporter PSC cell lines to monotorize and identify specific metabolic pathways and epigenetic marks throught differentiation process towards metanephric mesenchyme cells.

The information gained from this model will offer improved insight into disease pathology and progression. The model may also serve as a tool for drug discovery to identify therapeutic targets and nephrotoxicity. In the future, this model can be combined with other kidney structures and inflammatory cells to engineer a more complete kidney and more extensively model kidney diseases.