Cardiovascular Pathobiology

Dwight Towler to lead Pathobiology Program

Dwight Towler to lead Pathobiology Program

Dwight A. Towler, M.D., Ph.D. has joined Sanford-Burnham's Lake Nona campus as professor and director of the Cardiovascular Pathobiology Program.

Heart hormone helps shape fat metabolism

Heart hormone helps shape fat metabolism

A study at Sanford-Burnham suggests that the heart plays a role in breaking down fat. Sheila Collins, Ph.D. and colleagues observed how hormones released by the heart stimulate fat cell metabolism.

The many flavors of diabetic heart disease

The many flavors of diabetic heart disease

The diabetic heart is different from the non-diabetic failing heart in that it is filled with fat.

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Studying cardiovascular pathobiology

Scientists in the Cardiovascular Pathobiology Program conduct research on fundamental and early translational aspects of cardiovascular biology, physiology, and disease. High blood pressure (hypertension), heart injury, and diabetes all lead to a thickening and weakening of the heart muscle, leading to fibrosis and progressive dilatation of the ventricles. Similarly, hypertension, smoking, high cholesterol levels, and diabetes can all contribute to atherosclerosis and heart attack. Distinct signatures of the underlying disease processes may exist at the cellular level, but it is often difficult to point to a specific reason for heart failure and vascular disease. This is especially true in obese or diabetic patients, given that high blood pressure and heart disease together with metabolic disturbances often coexist. Moreover, in certain diseases, such as chronic kidney disease (CKD), diabetes and/or hypertension are caught up in a “perfect storm” of blood-vessel inflammation and destruction, driven by systemic changes in phosphate and mineral metabolism. These changes drive arteriosclerotic calcification and the risk of stroke, heart attack, congestive heart failure, lower extremity amputation, and sudden death.

Your Health

In order to treat heart and vascular diseases at the earliest stages, the underlying pathogenic mechanisms must be understood. An objective of the program is to conduct fundamental and translational studies that will lead to greater insight into specific heart failure, valvular, and arteriosclerotic vascular disease, leading to informed and individualized treatments. The mission of the program comprises three major components:

  • Mechanisms of Disease - Program scientists are researching pathogenic mechanisms involved in the development of cardiac dysfunction. Similar studies will be conducted for vascular disease. The program will support studies from fundamental experimental model systems to humans. This goal demands enhancement of research expertise in bioengineering, metabolite sensing, biorepository development, and human disease epigenetics via strategic faculty recruitment and external collaborations.
  • Biosignatures/biomarkers - Fundamental studies of mechanism will be tied to the identification of biochemical, genetic, or imaging-based biomarkers that define specific cardiovascular diseases. Systems-based metabolomic, lipidomic, genomic, and epigenomic strategies will be employed to define relevant biosignatures, a first step toward biomarker discovery. This goal demands a strong research technology platform and links with clinical research programs evolving with key health-care collaborators.
  • Therapeutic targets - Mechanistic studies, combined with molecular profiling, shows promise for the identification of candidate molecules and pathway targets for new therapies. The new treatments will be aimed at the early stages of disease and individualized to the specific cardiovascular disease. The search for new therapeutics will utilize the power of small-molecule and functional genomic screening using extensive cellular phenotyping, metabolomics, and genomic profiling as endpoints. Program scientists will also explore biologic and RNA/DNA-based therapeutic strategies.

Research - Diabetes and Obesity - Cardiovascular Pathobiology: How Our Research Helps

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Hard at work against the hardening of arteries

Sanford-Burnham researchers identified a potential drug target to prevent the hardening of arteries in patients with atherosclerosis. The gene Dkk1 encodes a protein that plays a key role in increasing the population of connective-tissue cells during wound repair, but prolonged Dkk1 signaling in cells lining blood vessels can lead to fibrosis and a stiffening of artery walls.  Read More...
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