Inflammation is one of the immune system's most important defenses. When the body detects an infection or injury, it sends out alarm signals that recruit immune cells and other cells to eliminate the threat and begin repairing damaged tissue. This response is essential, but it is supposed to shut down once the danger has passed.
As people age, however, certain cells accumulate that can keep inflammation active for much longer than necessary. This persistent inflammation has been associated with numerous diseases that become more common later in life. Researchers at Sanford Burnham Prebys Medical Discovery Institute, Mayo Clinic, and collaborating institutions have now uncovered a previously unknown connection between mitochondria, cell metabolism, and this chronic inflammation.
Their findings, published in Nature, also showed that interfering with part of the process reduced inflammation and supported healthier aging in mice. Many cells in the body are capable of dividing, allowing us to grow and helping tissues repair themselves after injury. But as we get older, increasing numbers of cells enter a state known as senescence.
These zombie-like senescent cells stop dividing, yet they remain alive and active. "Senescent cells are not completely inert," said co-corresponding author Peter Adams, PhD, the Jeanne and Gary Herberger Leadership Chair in Cancer Research at Sanford Burnham Prebys. Adams also is director of and professor in the Cancer Genome and Epigenetics Program.
"They remain metabolically active and have an inflammatory program causing them to secrete inflammatory molecules." When senescent cells activate this inflammatory program, they are described as having the senescence-associated secretory phenotype (SASP). SASP has been linked to widespread inflammation associated with aging as well as a range of chronic diseases. The research team, led by the laboratory of senior and co-corresponding author João Passos, PhD, a professor of Physiology at Mayo Clinic, set out to identify the molecular processes that drive SASP.
Their broader goal was to determine whether those processes might be interrupted or reduced. "It turns out that there is a convergence of at least two biological pathways related to mitochondria," said Adams. "One alters how DNA is stored to promote areas related to SASP, and the other boosts the expression of the exposed SASP genes." Mitochondria Help Unlock Inflammatory Genes Although senescent cells no longer divide, they continue using energy and carrying out metabolic activity.
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