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Active NON-SBIR/STTR RPGS NIH (US)

Building Healthy Habits for Heart Health

$2.43M USD

Funder NATIONAL INSTITUTE ON MINORITY HEALTH AND HEALTH DISPARITIES
Recipient Organization University of Cincinnati
Country United States
Start Date Sep 23, 2024
End Date Jun 30, 2029
Duration 1,741 days
Number of Grantees 1
Roles Principal Investigator
Data Source NIH (US)
Grant ID 10857634
Grant Description

PROJECT SUMMARY Vascular calcification is the major precursor to cardiovascular disease and is further exacerbated by chronic kidney disease. Black or African Americans are more than 3 times as likely and Hispanics or Latinos are 1.3 times more likely to have kidney failure compared to White Americans. In addition to Black Americans having higher rates of

heart and kidney diseases, they also often live in rural or impoverished areas that are food deserts. Low-income areas are more than often communities with a lack of access to healthy foods, otherwise known as food deserts. Heart disease and other CVCs such as chronic kidney disease, Stroke, and etc are the leading cause of death for African-

Americans, more so African-American males. While phosphate is a natural element that is found in meat and dairy products, it is also a known precursor to vascular calcification which leads to the onset of CVCs and other complications. The levels of phosphate in industrially processed foods and meats are found to be much higher than levels in fresh

produce. Increased serum levels of inorganic phosphate leads to calcification of vascular smooth muscle cells and a phenotypic switch to an osteoblast-like cell. Once thought to be a passive process of calcium and phosphate deposition within arteries, vascular calcification is now known to be an active, cell-regulated condition. There is a

clinical need to develop a therapy for vascular calcification that reduces calcification without causing arterial damage similar to current therapies such as endovascular stent and atherectomy. This project will examine the role of phosphate in vascular smooth muscle cell calcification and the potential of protein therapy to reduce calcification. The

proposed protein therapy would include reestablish fetuin-A to its native levels to treat smooth muscle cell calcification in patients with the comorbidities of heart disease and chronic kidney disease. Fetuin-A forms in the liver, gets released into the blood stream, then stabilizes free calcium-phosphate clusters into calciprotein particles that are filtered

from the blood by the kidneys and excreted through urine. Through a collaboration with MSU Extension we will work to increase the diversity of the biomedical workforce while allowing the participants to give back to their communities and help older generations.

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University of Cincinnati

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