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BMS Professor Awarded $1.8 Million NIH Grant to Study Calcium Channel Functions and Cardiovascular Disease

Dr. Gregory Amberg, Associate Professor in the Department of Biomedical Sciences was recently awarded a $1.8 million grant from the National Institute of Health to study calcium channel function in arterial smooth muscle.

The five-year research project hopes to shed light on how oxidant and calcium signals influence blood vessel functions that regulate blood flow and pressure –functions that could contribute to cardiovascular diseases such as hypertension, stroke, and coronary artery disease.

Cardiovascular disease is the leading cause of death in the United States – at a rate of 30-40% – and carries with it a huge economic cost. Coronary heart disease alone cost the United States almost $109 billion per year.

“Hypertension is one of the major modifiable risk factors for cardiovascular disease, but often goes undiagnosed until it is in the more advanced stages where the damage is already done,” said Dr. Amberg. “My research is showing that there is a linked, reciprocal relationship between two fundamental cell signaling modalities – oxidation and calcium influx - and that increases in these signals may be early events involved with the development of hypertension.”

Two hallmarks of vascular dysfunction are enhanced generation of reactive oxygen species and enhanced calcium influx. One area that isn’t very well known in any cell type is redox or oxidative signaling and its relationship to calcium signaling – an area that Amberg plans to focus on.

“Oxidative stress is generally known to be detrimental to cell function - it is involved with cell damage and death which contributes to tissue modifications associated with various pathologies – however, it is also part of the normal physiology of many cell types,” said Dr. Amberg. “I’m trying to understand how reactive oxygen species operate in healthy cells and identify the events that underlie the transition from normal oxidative signaling to overt oxidative stress in pathophysiological conditions associated with disease.”