{
  "id": 6446988,
  "title": "Removing inflammation-linked protein makes aging worse",
  "url": "https://urgent.news/2026/09/09/removing-inflammation-linked-protein-makes-aging-worse",
  "topic": "health",
  "section": "Health & Medicine",
  "published": "2026-09-09T17:20:39.000Z",
  "source": {
    "name": "Futurity",
    "slug": "futurity",
    "url": "https://www.futurity.org/cgas-protein-inflammation-aging-3344842/"
  },
  "original_language": "en",
  "account": "Researchers have discovered that cGAS, a protein involved in triggering inflammation, also serves a protective function. At the University of Rochester, scientists initially thought blocking the protein might slow aging. However, they found the opposite: mice lacking cGAS became weaker, more inflamed, and lived shorter lives. This finding reveals that cGAS has two opposing roles. It can cause inflammation when it encounters DNA in the wrong place inside a cell. Yet, researchers also discovered it helps prevent chronic inflammation associated with aging and age-related diseases. The results, published in Nature Aging, could impact the development of treatments targeting age-related inflammation. Contrary to expectations, removing cGAS led to faster aging in mice. Researchers knew cGAS played a role in inflammation, activating STING when DNA is detected in the cytoplasm. Together, cGAS and STING form the cGAS-STING pathway, which is linked to aging and inflammation. By removing cGAS from mouse models, the team unexpectedly found another side to the protein. Inside the nucleus, cGAS helps maintain chromatin, packaging DNA tightly and suppressing genetic elements called LINE1s. Without cGAS, these normally suppressed elements become more active. This can lead to LINE1-derived DNA entering the cytoplasm, where cells might mistake it for a threat and trigger inflammation. In essence, cGAS has two seemingly opposing jobs: outside the nucleus, it acts as an alarm system, detecting misplaced DNA and activating inflammation. Within the nucleus, cGAS helps prevent some of that inflammatory DNA from being produced in the first place. Inflammation is the body's natural response to injury or infection, beneficial in young, healthy individuals. However, persistent inflammation can damage cells and tissues as people age, contributing to diseases like cancer, cardiovascular issues, and neurodegenerative disorders. Chronic inflammation within our DNA—primarily from transposable elements like LINE1s—can become more active with aging, leading to inflammation. While cGAS can trigger inflammation, it also helps control this inflammatory process. These findings pose a challenge for scientists aiming to combat age-related inflammation by targeting cGAS. Blocking or eliminating cGAS might reduce one source of inflammation, but it could also remove a protective mechanism against another inflammatory source. Therefore, future therapies might need to preserve cGAS's protective role in the nucleus while blocking its inflammatory activity elsewhere, according to Vera Gorbunova, a biology professor and center director at the University of Rochester.",
  "summary": "New findings could have implications for developing treatments and therapies designed to target age-related inflammation.",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}