Apr 7, 2026
- Erik Blackwood, PhD, received two NIH R01 grants totaling $7.4 million
- The funding supports research on heart failure with preserved ejection fraction (HFpEF), which affects half of all heart failure patients
- Blackwood’s work focuses on understanding disease causes and developing new treatments
Erik Blackwood, PhD, assistant professor in the Department of Nutrition & Integrative Physiology and investigator in the Nora Eccles Harrison Cardiovascular Research & Training Institute (CVRTI) and the Diabetes & Metabolism Research Center at the University of Utah College of Health, has received two National Institutes of Health (NIH) R01 grants totaling $7.4 million. Both grants were awarded in fall 2025 and support research focused on cardiometabolic disease and heart failure with preserved ejection fraction (HFpEF), one of the most common and challenging forms of heart failure.
HFpEF affects about half of all people with heart failure. In this condition, the heart can still pump blood, but it has trouble relaxing and filling with blood between beats. This makes it harder for oxygen and nutrients to reach the body. Many people with HFpEF also have other health problems, such as obesity, type 2 diabetes, and high blood pressure. These combined conditions often make people feel very sick and can shorten their lives. Currently, there are no proven treatments that directly fix HFpEF, making it a major unmet need in heart medicine.
One NIH-funded project studies how the heart and liver work together to affect overall health. Blackwood’s team is focusing on a protein called serum glucocorticoid kinase 1 (SGK1), which may help the heart send signals to the liver. These signals could influence how the body handles sugar and fat. This is important because many people with HFpEF also have fatty liver disease, which can make heart failure worse and increase the risk of death. By understanding this heart–liver connection, researchers hope to find new ways to treat both heart failure and metabolic disease at the same time.
The second project looks at how scar tissue forms in the heart. When the heart is under stress for a long time, it can become stiff due to excess scar tissue, making it harder to beat normally. This scarring also raises the risk of dangerous heart rhythm problems. Blackwood’s lab is studying a protein called IRE1, which appears to control how heart cells respond to stress and how scar tissue develops. By targeting IRE1, the team hopes to design new treatments that can slow down or prevent harmful scarring in the heart.
Together, these two projects aim to move discoveries from the lab toward real-world treatments. By learning what causes HFpEF and how it affects the body, Blackwood’s research could lead to new therapies that help patients live longer and feel better.
Blackwood joined the University of Utah in 2024 as a tenure-line assistant professor. Born and raised in San Diego, he earned his bachelor’s degree from the University of Notre Dame, where he studied cardiovascular physiology. He later worked as a first responder and emergency medical technician before completing his PhD in cell and molecular biology with a focus on heart disease. His laboratory, housed in the CVRTI, now includes graduate students and postdoctoral researchers working together in a team-based environment. By combining basic science with treatment-focused research, Blackwood and his team are well positioned to advance new therapies toward future clinical trials.