A novel relationship between feeding behavior and coagulation factor 11 (F11) in HFpEF
Description: Heart failure with preserved ejection fraction (HFpEF) accounts for approximately half of all heart failure cases globally. Given the complexity of the disease, effective therapies have been difficult to develop. Using system genetics, we were able to identify novel endocrine factors mediating liver-heart crosstalk in the hybrid mouse diversity panel (HDMP). We recently validated that liver-heart communication is mediated by coagulation factor 11 (F11) to protect against HFpEF progression partly by influencing circadian biology. We aim to further study the relationship between F11 and circadian rhythm in HFpEF. Multiple studies have shown that time-restricted feeding (TRF) ameliorates obesity, hyperlipidemia, and diabetes development. Since HFpEF is typically a secondary disease to obesity, hyperlipidemia, and diabetes, we propose that TRF could prevent HFpEF progression. Furthermore, we have evidence showing that F11 bioavailability is dependent on dietary changes. We propose that TRF will coordinate the F11 response to provide its effects on HFpEF.
Funder: American Heart Association
Amount: $67,390
Funding type: training
Funder scheme: Predoctoral Fellowship
Start date: 2024-04-01
End date: 2026-04-01
Investigators: Lorna Mendoza, Lorna Mendoza
Institution: The Regents of the University of California, Los Angeles
Subfield: Endocrine and Autonomic Systems
Field: Neuroscience
Domain: Life Sciences
Funded outputs count: 0
Funder award ID: 24PRE1198954
OpenAlex ID: G7958095591