{
  "id": 28441,
  "title": "Mitochondrial–Epigenetic Pathway Linked to Age-Related Inflammation",
  "url": "https://urgent.news/2026/07/30/mitochondrial-epigenetic-pathway-linked-to-age-related-inflammation",
  "topic": "health",
  "section": "Health & Medicine",
  "published": "2026-07-30T18:37:27.000Z",
  "source": {
    "name": "GEN Biotechnology",
    "slug": "gen-biotechnology",
    "url": "https://www.genengnews.com/topics/translational-medicine/mitochondrial-epigenetic-pathway-linked-to-age-related-inflammation/"
  },
  "original_language": "en",
  "account": "Researchers have discovered a mechanism that links aging cells to chronic inflammation, a key factor in many age-related diseases. The study, published in Nature, reveals how dysfunctional mitochondria interact with the cell's epigenetic machinery to activate inflammatory genes. The accumulation of senescent cells, which continue to function metabolically despite no longer dividing, contributes to inflammation through the release of a mixture of inflammatory molecules called the senescence-associated secretory phenotype (SASP). This inflammation is believed to play a role in various conditions, including frailty, cardiovascular disease, cancer, neurodegeneration, and more.\n\nThe research, conducted by teams at Mayo Clinic and Sanford Burnham Prebys Medical Discovery Institute, builds upon earlier work by lead author João Passos, PhD. Passos' lab had previously shown that damaged mitochondria release their DNA and RNA into cells, triggering inflammatory pathways. The current study uncovers an additional, independent pathway that is equally critical. According to first author Helene Martini, PharmD, PhD, \"Inflammatory signaling alone isn't enough. The cells also require a metabolic signal from mitochondria that alters how inflammatory genes are turned on.\"\n\nThe researchers found that senescent cells produce more acetyl-CoA, a crucial molecule that can be generated from various sources but is primarily derived from mitochondria in these cells. This acetyl-CoA enables epigenetic modifications that make inflammatory genes more accessible for expression. Essentially, \"dysfunctional mitochondria can promote inflammation by controlling epigenetic switches that turn inflammatory genes on,\" Martini explained. Furthermore, the team identified a potential therapeutic target by discovering that blocking a mitochondrial citrate transporter called SLC25A1 reduces the supply of acetyl-CoA, thereby limiting histone acetylation at sites of SASP and inhibiting inflammatory gene activation, even when initial immune signals are still present. This finding suggests that modulating metabolic inputs into chromatin regulation could be a viable strategy to mitigate age-associated inflammation and functional decline.",
  "summary": "Crosstalk between mitochondrial metabolism and epigenetic regulation helps activate the inflammatory SASP in senescent cells, revealing a potential therapeutic target for limiting chronic inflammation during aging. The post Mitochondrial–Epigenetic Pathway Linked to Age-Related Inflammation appeared first on GEN - Genetic Engineering and Biotechnology News .",
  "key_points": [
    "Mitochondrial dysfunction links aging cells to chronic inflammation",
    "Senescent cells release inflammatory molecules called SASP",
    "Blocking SLC25A1 transporter reduces inflammation"
  ],
  "editors_take": null,
  "illustration": "https://urgent.news/ill/28441.png",
  "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."
}