{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T21:24:48Z","timestamp":1790889888757,"version":"4.1.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":4626,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2003,1]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Previous studies have shown that haploinsufficiency of the splanchnic and septum transversum mesoderm Forkhead Box (Fox) f1 transcriptional factor caused defects in lung and gallbladder development and that <jats:italic toggle=\"yes\">Foxf1<\/jats:italic> heterozygous (+\/\u2212) mice exhibited defective lung repair in response to injury. In this study, we show that Foxf1 is expressed in hepatic stellate cells in developing and adult liver, suggesting that a subset of stellate cells originates from septum transversum mesenchyme during mouse embryonic development. Because liver regeneration requires a transient differentiation of stellate cells into myofibroblasts, which secrete type I collagen into the extracellular matrix, we examined <jats:italic toggle=\"yes\">Foxf1<\/jats:italic> +\/\u2212 liver repair following carbon tetrachloride injury, a known model for stellate cell activation. We found that regenerating <jats:italic toggle=\"yes\">Foxf1<\/jats:italic> +\/\u2212 liver exhibited defective stellate cell activation following CCl<jats:sub>4<\/jats:sub> liver injury, which was associated with diminished induction of type I collagen, \u03b1-smooth muscle actin, and Notch-2 protein and resulted in severe hepatic apoptosis despite normal cellular proliferation rates. Furthermore, regenerating <jats:italic toggle=\"yes\">Foxf1<\/jats:italic> +\/\u2212 livers exhibited decreased levels of interferon-inducible protein 10 (IP-10), delayed induction of monocyte chemoattractant protein 1 (MCP-1) levels, and aberrantly elevated expression of transforming growth factor \u03b21. In conclusion, <jats:italic toggle=\"yes\">Foxf1<\/jats:italic> +\/\u2212 mice exhibited abnormal liver repair, diminished activation of hepatic stellate cells, and increased pericentral hepatic apoptosis following CCl<jats:sub>4<\/jats:sub> injury.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1053\/jhep.2003.50005","type":"journal-article","created":{"date-parts":[[2003,2,5]],"date-time":"2003-02-05T02:43:33Z","timestamp":1044413013000},"page":"107-117","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":118,"title":["Foxf1 +\/\u2212 mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injury"],"prefix":"10.1097","volume":"37","author":[{"given":"Vladimir 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