Paracrine cellular senescence exacerbates biliary injury and impairs regeneration - Ferreira-Gonzalez, Sofia; Lu, Wei-Yu; Raven, Alexander; Dwyer, Benjamin; Man, Tak Yung; O’Duibhir, Eoghan; Lewis, Philip J. Starkey; Campana, Lara; Kendall, Tim J.; Bird, Thomas G.; Tarrats, Nuria; Acosta, Juan-Carlos; et al. (Nature communications, 2018)
Keywords: 13; 13/1; 13/2; 13/51; 14/1; 14/19; 14/32; 14/63; 38/77; 45/90; 631/80/304; 631/80/509; 64; 64/60; 692/4020/4021/1607/1605; 692/4020/4021/44/1327; 82/80; Animals; Bile ducts; Bile Ducts - injuries; Bile Ducts - pathology; Cell cycle; Cells, Cultured; Cellular Senescence - physiology; Cholangitis, Sclerosing - pathology; Cholangitis, Sclerosing - therapy; Clonal deletion; Collagen; Collagen - metabolism; Disease control; Disease Models, Animal; Female; Gene deletion; Hepatocytes; Hepatocytes - pathology; Humanities and Social Sciences; Humans; Keratin-19 - genetics; Liver; Liver - pathology; Liver Cirrhosis, Biliary - pathology; Liver Cirrhosis, Biliary - therapy; Macrophages; Macrophages - metabolism; Male; MDM2 protein; Mice; Mice, Inbred C57BL; Mice, Knockout; multidisciplinary; Myofibroblasts - metabolism; Paracrine signalling; Proto-Oncogene Proteins c-mdm2 - genetics; Regeneration; Regeneration - physiology; Rodents; Science; Science (multidisciplinary); Senescence; Therapeutic applications; Transforming Growth Factor beta1 - antagonists & inhibitors; Transforming Growth Factor beta1 - metabolism; Viability