The human gut is remarkable. It produces new cells every few days, thanks to special stem cells that keep everything running smoothly. However, as we age, these stem cells gather changes in their DNA that can affect their functions. These changes act like switches, turning genes on and off.
A recent study published in Nature Aging, led by Prof. Francesco Neri from the University of Turin, reveals a pattern in these changes. They found something called ACCA, short for Aging- and Colon Cancer-Associated drift. This drift becomes stronger as we age, and it’s important because it shows a clear epigenetic pattern that links aging with health issues.
The genes that are most affected help maintain the balance in our guts. They are crucial for repairing the intestinal lining. When these genes change, our gut’s healing ability declines. The research indicates that this drift isn’t just seen in aging tissue but also in colon cancer samples, suggesting that older stem cells may make it easier for cancer to develop.
Interestingly, aging doesn’t affect the gut uniformly. The gut consists of tiny structures called crypts, each stemming from a single stem cell. When a stem cell undergoes changes, all the cells in that crypt inherit those changes. Dr. Anna Krepelova explains that over time, areas with older profiles expand, leading to patches of both young and aged cells within the gut. This mix can increase the risk of cancer; some areas remain healthy, while others may produce damaged cells.
Researchers also discovered why this drift occurs. Aging intestinal cells absorb less iron and release more. This impacts iron’s availability in the nucleus, which is necessary for TET enzymes that help clear out excess DNA markings. When there’s not enough iron, these enzymes can’t function properly. As a result, unwanted markings stay on the DNA, ultimately leading to the silencing of key genes.
Inflammation in the gut compounds these issues. Even mild inflammation can disrupt iron balance, putting additional stress on gut cells and weakening their signaling. This combination of iron imbalance and inflammation speeds up the aging process in the intestine.
However, not all hope is lost. In lab tests using organoids—tiny models of intestines created from stem cells—researchers found they could slow or partially reverse the epigenetic drift. By restoring iron intake or boosting signaling pathways, they reactivated the TET enzymes, allowing cells to clear out excess DNA markings. Dr. Krepelova emphasizes that this shows aging isn’t a fixed state; we have the potential to influence it at a molecular level.
In summary, the study reveals that as our guts age, they become a patchwork of old and young cells, which can increase cancer risk. By understanding and addressing these changes—especially related to iron balance and inflammation—we might be able to slow down or even reverse some aging effects in the gut. As research continues, the hope is that we can use these findings for better health as we age.
For more insights, you can check Nature Aging.
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