{
  "id": 18027152,
  "title": "An Ovol1 Variant in Endothelial Cells Regulates Slug and is Essential for Pathological Angiogenesis",
  "url": "https://urgent.news/2026/11/03/an-ovol1-variant-in-endothelial-cells-regulates-slug-and-is-essential",
  "topic": "science",
  "section": "Science",
  "published": "2026-11-03T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.10.31.763143v1?rss=1"
  },
  "original_language": "en",
  "account": "During development, blood vessels expand via a process called sprouting angiogenesis. However, when this process becomes dysregulated, it can lead to pathological angiogenesis in diseases such as neovascular conditions, causing excessive, disorganized blood vessels. Research previously discovered that a transcription factor called Slug, acting as a pro-mesenchymal factor, plays a crucial role in angiogenesis by orchestrating an endothelial-to-mesenchymal transition (pEndoMT). The mechanisms behind how Slug is activated and how it contributes to diseases remain unclear. A new study reveals that endothelial cells possess a rare low molecular weight variant of Ovol1, a zinc-finger transcription factor that governs mesenchymal transition in epithelial cells. Ovol1 and Slug are co-expressed in angiogenic endothelial cells, and the research confirms that Ovol1 directly binds to the endogenous Slug gene at a region common across species. Unexpectedly, endothelial Ovol1 variant upregulates Slug and is responsible for driving pEndoMT marker expression, enhancing endothelial cell migration. Silencing Ovol1 disrupts sprouting angiogenesis in a 3D in vitro model, while overexpression of Ovol1 results in excessive, disorganized sprouting, all dependent on Slug. Mice lacking Ovol1 or Slug in endothelial cells (Ovol1ECKO and SlugECKO) showed normal neonatal retinal angiogenesis but experienced aggressive, disorganized sprouting in adulthood. In adulthood, Ovol1 levels decreased in established blood vessels but increased strongly in tumor endothelial cells, reducing colorectal cancer syngraft growth alongside hindering tumor angiogenesis. Furthermore, neovascularization in the oxygen-induced retinopathy (OIR) model was diminished in SlugECKO mice. The study concludes that an endothelial Ovol1 variant boosts Slug and initiates a mesenchymal-like state, making the Ovol1-Slug pEndoMT signaling axis vital for pathological angiogenesis in neovascular disease models.",
  "summary": "During development, the blood vasculature expands by sprouting angiogenesis, but the programs that guide this process can become dysregulated in the pathological angiogenesis of neovascular diseases leading to excessive disorganized blood vessels. We previously reported that in endothelial cells, the pro-mesenchymal transcription factor Slug critically regulates angiogenesis through a partial and…",
  "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."
}