Fat cells fuel artery plaque via inflammation
Atherosclerosis is the leading cause of death worldwide. New research suggests that fat cells play a more active role than previously thought, sending inflammatory signals to blood vessel walls that accelerate plaque growth.
Fat tissue is often seen as passive storage. But fat cells (adipocytes) are hormonally active. They secrete substances that can fuel inflammation and oxidative stress, both locally and throughout the body. This process appears to contribute to the buildup of fatty deposits (plaques) in artery walls, a condition known as atherosclerosis.
What the study did
Researchers focused on a specific signalling protein in fat cells: the NKA alpha-1 subunit (Na/K-ATPase). This protein activates a cascade that increases oxidative stress and inflammatory activity. By expressing an inhibitory peptide called NaKtide exclusively in fat cells, they could test what would change.
They used mice lacking the APOE gene, which rapidly develop atherosclerosis on a Western diet. Animals receiving the inhibitory peptide showed substantially less plaque after twelve weeks: 67 percent less in the aortic arch and 48 percent less at the aortic sinus. The study was published in Arteriosclerosis, Thrombosis, and Vascular Biology.
Fat tissue as an inflammatory source
Beyond reduced plaque, other markers also improved. Inflammation in fat tissue itself decreased, glucose tolerance improved, and systemic inflammation fell. The number of macrophages (immune cells that help build plaques) in the vessel wall also declined.
From a longevity perspective, this is noteworthy. Chronic low-grade inflammation, often called inflammaging, is considered one of the central drivers of ageing. Fat tissue that secretes inflammatory substances may sustain that background inflammation over time.
The researchers emphasise that these results were obtained in animal models. Whether the NaKtide mechanism can also reduce atherosclerosis in humans remains unknown. These findings are preliminary and require further research in human cells and, ultimately, clinical trials.
Search terms to explore further: adipocyte NKA signaling atherosclerosis | inflammaging adipose tissue | oxidative stress vascular plaque formation