(Boston)—As organisms grow, older cells can undergo a phenomenon called senescence. This process defines a cell state where cells permanently stop dividing but do not die. Senescent cells secrete toxic pro-inflammatory factors contributing to the development of many diseases.
Researchers from Boston University School of Medicine (BUSM) have shown that obesity in experimental models led to senescence of macrophages, an immune cell subtype within fat or adipose tissue.
According to the researchers, the fact that macrophages can become senescent is an unexpected finding. Many of the macrophages within obese tissue were senescent and those senescent cells may be a significant driver of fat tissue fibrosis. These findings suggest that obesity accelerates cellular or biological immune aging in fat.
"In healthy individuals, those cells contribute to cleaning the tissue from dead adipocytes (cells specialized for the storage of fat) and help in the cellular turnover. We demonstrated that macrophages lost this capacity when they become senescent," explained first and co-corresponding author Nabil Rabhi, PhD, an instructor of biochemistry at BUSM.
Collaborators from BUSM included co-corresponding authors Matthew D. Layne, PhD, associate professor of biochemistry and assistant dean for research and Stephen R. Farmer, PhD, professor of biochemistry.
These findings appear online in the journal Life Science Alliance.
Funding for this study was provided by the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (DK117161 and DK117163 to SRF), the American Heart Association (AHA) fellowship (17POST33660875 to NR) and The Evans Center for Interdisciplinary Biomedical Research ARC on "Connecting Tissues and Investigators, Fibrosis in Pathology" at Boston University.
