{
  "abstract": "Endothelial-to-mesenchymal transition (EndMT) is a cell trans-differentiation process which occurs during embryonic development as well as in a variety of pathological contexts. During this process, cells lose their endothelial lineage markers and gain mesenchymal ones. It is stimulated by several factors, such as TGF-β, high glucose, or hypoxia, which trigger intracellular pathways, mainly the Smad and ERK pathways, leading to modulation of transcription factors. While Ca 2+ signaling is known to participate in a wide variety of cellular processes, its role in the context of EndMT is only partially understood, although several Ca 2+ -carrying and Ca 2+regulated proteins have been shown to influence EndMT. These include Ca 2+ -permeable channels from the mechanosensitive Piezo family and members of the TRP family; the actors involved in store-operated Ca 2+ entry, including IP 3 -receptors located on the endoplasmic reticulum membrane, the endoplasmic reticulum Ca 2+ sensor STIM1, and the Ca 2+ -permeable plasma membrane channel Orai1; the mitochondrial Ca 2+ uniporter complex; Ca 2+ -activated channels such as the non-selective monovalent cation channel TRPM4 and the big-conductance K + channel BK Ca ; Ca 2+ -regulated signaling pathways such as the Ca 2+ -calmodulin-calcineurin-NFAT pathway and the calpain-ERK pathway.\n\nAfter a brief description of Ca 2+ signaling in endothelial cells, this review will specifically detail the available data on the Ca 2+ signaling in EndMT. Links between Ca 2+ signaling and other signaling pathways leading to EndMT will be discussed. Finally, molecular targets that may be valuable to explore in order to prevent EndMT will be highlighted.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 6,
  "authors": [
    {
      "name": "Romain Guinamard"
    },
    {
      "name": "Corentin Kerevel"
    },
    {
      "name": "Anaïs Darengosse"
    },
    {
      "name": "Valentin Platel"
    },
    {
      "name": "Laurent Sallé"
    },
    {
      "name": "Christophe Simard"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/0ttz51frgvddz.bib",
  "cited_by": 0,
  "doi": "10.1016/j.ceca.2026.103163",
  "fulltext_url": null,
  "id": "0ttz51frgvddz",
  "issns": [
    "0143-4160",
    "1532-1991"
  ],
  "landing_url": "https://hal.science/hal-05733195v1",
  "language": "en",
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "hal",
      "0.sdv"
    ],
    [
      "openalex",
      "2809|Ion Channels and Receptors"
    ]
  ],
  "openalex": "W7165633038",
  "pdf_url": "https://hal.science/hal-05733195/document",
  "pmcid": null,
  "pmid": null,
  "published": "2026-06-25",
  "publisher": "Elsevier",
  "ris": "https://research.draconitic.com/paper/0ttz51frgvddz.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:24Z",
      "native_id": "hal-05733195",
      "source": "hal",
      "url": "https://hal.science/hal-05733195v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "openalex:2809|Ion Channels and Receptors",
      "subfield": "neuroscience"
    }
  ],
  "title": "Molecular actors of the Calcium signaling in the endothelial-to-mesenchymal transition: poorly explored therapeutic targets",
  "title_text": "Molecular actors of the Calcium signaling in the endothelial-to-mesenchymal transition: poorly explored therapeutic targets",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:24Z",
  "url": "https://research.draconitic.com/paper/0ttz51frgvddz",
  "venue": "Cell Calcium",
  "versions": []
}