Heart failure with preserved ejection fraction (HFpEF) is a common and serious form of heart failure, accounting for at least half of all cases. Up to 5% of Americans are believed to have HFpEF, with much higher rates in older adults. Despite advances in care, more than half of those diagnosed with HFpEF die within five years. We often think of heart failure as a problem of the heart alone, but HFpEF is a whole-body disease. One of the most important and overlooked players are skeletal muscles. In HFpEF, these muscles become weak and tired more easily. People feel exhausted, so they move less. Moving less further weakens the muscles and worsens heart health, creating a vicious cycle that accelerates chronic disease.

My research focuses on understanding how and why skeletal muscle becomes dysfunctional in HFpEF, and how those changes feed back to worsen heart disease. A key area of interest is proteostasis, the cell’s system for maintaining a healthy balance of proteins – making new ones, repairing damaged ones, and removing those that can’t be fixed. In aging and HFpEF, this quality-control system breaks down, leading to the buildup of damaged proteins that impair muscle function. By uncovering how disrupted proteostasis and abnormal muscle-to-heart signaling drive HFpEF, our goal is to identify new ways to keep muscles healthy, break the cycle of fatigue and inactivity and ultimately improve outcomes for people living with this form of heart failure.