The molecular mechanism(s) by which high glucose milieu constitutes an adverse in utero environment that impairs renal development and consequently programs the offspring to develop hypertension, renal dysfunction and cardiovascular disease.

Several transgenic mice and diabetic animal models are used to study of the functional impact and mechanism(s) in which a high glucose milieu leads to embryonic dysmorphogenesis, nephron deficiency, and long-term outcome (i.e., hypertension in adulthood). Advanced research approaches such as gene chip microarrays, micro-dissection and organ culture image analysis etc. cover a span of studies in vitro, ex vivo and in vivo.

Collaborations with researchers at the Harvard Medical School, McGill University, University of Toronto and Université de Montréal