Severe obesity reshapes the heart’s muscle proteins
In severe obesity, the heart works differently at the molecular level. A study in Science now shows exactly what changes inside the muscle cells themselves.
Heart failure in which the heart still contracts but pumps poorly (HFpEF, heart failure with preserved ejection fraction) is the fastest-growing form of heart disease worldwide. People with severe obesity face a substantially higher risk. But why the heart functions poorly in these patients was not well understood at the molecular level.
Researchers published an analysis in the journal Science of heart muscle cells from people with severe obesity. The study shows that the contractile proteins in those cells, the molecular motors that make the heart beat, are structurally altered. They are organized differently and function less efficiently than in people without obesity.
What exactly changes
The heart contracts through interaction between two proteins: myosin and actin. Myosin acts as a molecular motor, moving along actin filaments. In people with severe obesity and HFpEF, the organization of these proteins is disrupted. The muscle fibers contract differently, leading to reduced pumping capacity even when the heart appears outwardly normal.
This partly explains why HFpEF is so difficult to treat. Most existing heart medications were developed for heart failure where the heart pumps visibly weakly. In HFpEF, the underlying cause is fundamentally different.
Connection to aging
HFpEF primarily affects older people. Aging and obesity amplify each other’s effects on heart function. Both processes alter how muscle cells use energy and produce proteins. This research provides a more precise description of what goes wrong in the heart at the cellular level, which may aid in developing more targeted therapies.