{
  "id": 9851416,
  "title": "Lactate Receptor Activation Alleviates Senescence and Preserves Homeostasis of Aged Arteries",
  "url": "https://urgent.news/2026/09/25/lactate-receptor-activation-alleviates-senescence-and-preserves",
  "topic": "science",
  "section": "Science",
  "published": "2026-09-25T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.09.20.753049v1?rss=1"
  },
  "original_language": "en",
  "account": "Recent research has uncovered a key factor in the aging process of arteries. By examining the genetic makeup of human aortic tissue, scientists found that HCAR1, a gene encoding the lactate receptor GPR81, is significantly reduced as arteries age. This suggests that the loss of GPR81 contributes to vascular senescence, or aging, in the vessel walls.\n\nWhen researchers studied human endothelial and smooth muscle cells, they discovered that these cells accumulated harmful lipids, had increased labile iron, and experienced elevated levels of ferroptosis, a type of cell death. By silencing the GPR81 gene in young cells, these same metabolic issues and signs of senescence emerged. Furthermore, in young mice with their endothelial cells specifically lacking GPR81, the mice displayed signs of senescence, including poor lipid management, damaged endothelial function, and disrupted elastin.\n\nConversely, when researchers activated GPR81 using the compound CHBA, they observed a reversal of these detrimental effects. CHBA restored proper fatty acid metabolism, encouraged glycolytic reprogramming, and reduced ferroptotic stress and senescence-associated traits. In progeroid mice that carry a mutated form of the lamin A gene, CHBA treatment led to decreased arterial lipid buildup, reduced cellular senescence, improved vascular cell composition, enhanced endothelial function, and restored extracellular matrix homeostasis.\n\nOverall, this groundbreaking study demonstrates that the loss of GPR81 is a critical driver of vascular metabolic dysfunction and cellular senescence as arteries age. The researchers believe that pharmacological activation of GPR81 could be a promising therapeutic approach to preserve vascular homeostasis and combat age-related cardiovascular diseases.",
  "summary": "Arteries are among the first tissues to exhibit age-related dysfunction, yet the metabolic mechanisms driving vascular senescence remain poorly understood. Here, analysis of human aortic transcriptomic data identified HCAR1, encoding the lactate receptor GPR81, as one of the genes most significantly downregulated with age. We therefore investigated whether age-associated loss of GPR81 contributes…",
  "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."
}