The Abel Research Lab
Originated at Harvard Medical School in Boston in 1995, spent 13 years at the University of Utah between 2000 and 2013, then moved to the University of Iowa in 2013. Our current research interests focus on elucidating the molecular mechanisms leading to cardiac dysfunction in diabetes and the regulation of myocardial growth and metabolism by insulin signaling.
Our laboratory objectives include:
- Elucidating the molecular mechanisms that are responsible for cardiac failure in diabetes.
- Elucidating the molecular signals that coordinate the mitochondrial and metabolic adaptations to cardiac growth.
- Elucidating the mechanisms by which insulin and growth factor signaling regulate cardiac mitochondrial function and the adaptation of the heart to stress.
- Elucidating the role of mitochondrial dysfunction in the pathogenesis of insulin resistance, diabetes and its complications.
Our recent studies
Have underscored the importance of mitochondrial oxidative stress as a major mechanism leading to cardiac dysfunction in obesity and diabetes. Recent studies have focused on: (1) The contribution of excessive myocardial insulin signaling in the myocardium in accelerating left ventricular remodeling in the hypertrophied and failing heart. (2) The regulation of myocardial autophagy by insulin signaling. (3) The mechanisms by which myocardial lipid overload alters autophagy in cardiac muscle (4) The role of altered mitochondrial dynamics in the pathophysiology of cardiac dysfunction in obesity and insulin resistant states. (5) Mechanisms for increased thrombosis in obesity and insulin resistant states.