Investigating the biochemical mechanisms responsible for cardiovascular diseases, including ischemic heart disease and atherosclerosis.
Cardiovascular disease is the primary cause of death in the United States and determining the biochemical mechanisms responsible for the initiation and progression of cardiovascular diseases has been and remains an important public health concern in the United States and other industrialized nations.
We have directed our efforts towards identifying the biochemical mechanisms involved in alterations in lipid metabolism that occur during the inflammation that is the underlying driver of cardiovascular disease.
Our primary research interests are:
- microcirculatory dysfunction during sepsis
- ischemic heart disease
- systemic failure during halogen gas exposure
We use basic physiological models of myocardial disease, including coronary occlusion models, isolated perfused hearts, isolated adult cardiac myocytes, and murine atherosclerosis models, coupled with state-of-the-art instrumentation, such as GC-MS and ESI-MS analysis, to discover new biomolecules and mechanisms that mediate cardiovascular injury. We are also aligned with multiple clinical studies to ensure our basic science studies have clinical/human relevance.
Ongoing projects in the lab include:
- Examining a novel family of lipids, the chlorinated lipidomes, discovered by our lab to be biomarkers of cardiovascular disease as well as mediators of cardiovascular disease. These chlorinated lipids are produced as a result of the activation of leukocytes that infiltrate injured cardiovascular tissues during injury and produce the powerful oxidant, hypochlorous acid, which is responsible for the chemical reactions leading to chlorinated lipid production. We are examining the role of these lipids in myocardial ischemia, sepsis, and atherosclerosis.
- Identifying the lipid mediators produced following halogen gas exposure that elicit pronounced cardiovascular events leading to morbidity.
- Identifying phospholipases and phospholipase products that mediate injury in ischemic heart disease and atherosclerosis. Our previous studies have shown the activation of calcium-independent phospholipase A2 as an important mediator of ischemic injury and identified its translocation to membranes including nuclear membranes during myocardial ischemia.