Cells in humans and other complex organisms grow and divide. This process helps babies develop into adults. It also heals cuts and bruises. Sometimes, cells stop dividing and enter a state called senescence. Senescent cells act like zombies. They stay alive but cannot make new cells. As we age, these cells build up. Our immune system removes them, but it weakens over time.

Senescent cells do more than just stop growing. They start an inflammatory program. This means they release molecules that cause inflammation, a type of swelling and irritation in the body. Experts call this the senescence-associated secretory phenotype, or SASP. Too much SASP leads to chronic inflammation. Scientists name this “inflammaging.” Inflammaging connects to diseases like heart problems or arthritis that often come with age.

A new discovery about cell powerhouses

Researchers at Sanford Burnham Prebys have found something important. Their work is published in Nature Communications.

Mitochondria, the tiny powerhouses inside cells, play a role. They help a protein called p53 fix DNA and control SASP. When damaged, bits of DNA can leak into the cytoplasm. These bits, called cytoplasmic chromatin fragments or CCF, trigger SASP. The immune system sees this DNA as a threat.

The team made human cells senescent using radiation. They showed p53 stops SASP and CCF from forming. In mice, they used a drug to boost p53. This drug, originally for cancer, did not lower senescent cell numbers. Instead, it changed their behavior. It reduced the inflammation signs tied to aging. This could limit inflammaging.

The researchers also learned mitochondria in senescent cells fail. Weak mitochondria lead to more CCF and less p53. This creates a cycle that harms cells. In a Sanford Burnham Prebys press release, the scientists explain this connection. They say that p53 helps repair DNA and keeps inflammation in check. They also note that drugs can tweak this system. In lab tests and mice, these drugs worked. Someday, doctors could help humans age healthier by targeting p53.

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