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Understanding cell turnover rates\u2014the time between a cell\u2019s birth and death\u2014can shed light on stemness potential and susceptibility to damage. However, measuring turnover rates in human organs has been a significant challenge. In this study, we integrate transcriptomic data from both tissue and shed cells to assign turnover scores to individual cells, leveraging their expression profiles in spatially resolved expression atlases. By performing RNA sequencing on shed cells from the upper gastrointestinal tract, collected via nasogastric tubes, we infer turnover rates in the human esophagus, stomach, and small intestine. In addition, we analyze colonic fecal washes to map turnover patterns in the human large intestine. Our findings reveal a subset of short-lived, interferon-stimulated colonocytes within a distinct pro-inflammatory microenvironment. Our approach introduces a dynamic dimension to single-cell atlases, offering broad applicability across different organs and diseases.<\/jats:p>","DOI":"10.1038\/s44320-025-00154-w","type":"journal-article","created":{"date-parts":[[2025,10,2]],"date-time":"2025-10-02T16:02:38Z","timestamp":1759420958000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Transcriptomic profiling of shed cells enables spatial mapping of cellular turnover in human organs"],"prefix":"10.1038","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1323-8117","authenticated-orcid":false,"given":"Tal","family":"Barkai","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8849-6615","authenticated-orcid":false,"given":"Oran","family":"Yakubovsky","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yael","family":"Korem Kohanim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keren","family":"Bahar Halpern","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-5514-6047","authenticated-orcid":false,"given":"Sapir","family":"Shir","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noa","family":"Oren","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michal","family":"Fine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-2637-8517","authenticated-orcid":false,"given":"Paz","family":"Kelmer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3820-1305","authenticated-orcid":false,"given":"Amit","family":"Talmon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alon","family":"Israeli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Niv","family":"Pencovich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ron","family":"Pery","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ido","family":"Nachmany","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0685-2522","authenticated-orcid":false,"given":"Shalev","family":"Itzkovitz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,10,2]]},"reference":[{"key":"154_CR1","doi-asserted-by":"crossref","first-page":"600","DOI":"10.1038\/s41586-020-2003-8","volume":"578","author":"V Abadie","year":"2020","unstructured":"Abadie V, Kim SM, Lejeune T, Palanski BA, Ernest JD, Tastet O, Voisine J, Discepolo V, Marietta EV, Hawash MBF et al (2020) IL-15, gluten and HLA-DQ8 drive tissue destruction in coeliac disease. 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