{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T10:57:42Z","timestamp":1792148262670,"version":"4.4.0"},"edition-number":"1","reference-count":393,"publisher":"Wiley","isbn-type":[{"value":"9780470650714","type":"electronic"}],"license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Liver regeneration is perhaps the most studied example of compensatory growth aimed to replace loss of tissue in an organ. Hepatocytes, the main functional cells of the liver, manage to proliferate to restore mass and to simultaneously deliver all functions hepatic functions necessary to maintain body homeostasis. They are the first cells to respond to regenerative stimuli triggered by mitogenic growth factor receptors MET (the hepatocyte growth factor receptor] and epidermal growth factor receptor and complemented by auxiliary mitogenic signals induced by other cytokines. Termination of liver regeneration is a complex process affected by integrin mediated signaling and it restores the organ to its original mass as determined by the needs of the body (hepatostat function). When hepatocytes cannot proliferate, progenitor cells derived from the biliary epithelium transdifferentiate to restore the hepatocyte compartment. In a reverse situation, hepatocytes can also transdifferentiate to restore the biliary compartment. Several hormones and xenobiotics alter the hepatostat directly and induce an increase in liver to body weight ratio (augmentative hepatomegaly). The complex challenges of the liver toward body homeostasis are thus always preserved by complex but unfailing responses involving orchestrated signaling and affecting growth and differentiation of all hepatic cell types. \u00a9 2013 American Physiological Society.\n                    <jats:italic>Compr Physiol<\/jats:italic>\n                    3:485\u2010513, 2013.\n                  <\/jats:p>","DOI":"10.1002\/cphy.c120014","type":"other","created":{"date-parts":[[2012,12,10]],"date-time":"2012-12-10T12:35:06Z","timestamp":1355142906000},"page":"485-513","source":"Crossref","is-referenced-by-count":161,"title":["Principles of Liver Regeneration and Growth Homeostasis"],"prefix":"10.1002","author":[{"given":"George K.","family":"Michalopoulos","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,1]]},"reference":[{"key":"e_1_2_8_2_1","first-page":"G579","article-title":"Antibodies to tumor necrosis factor\u2010alpha inhibit liver regeneration after partial hepatectomy","volume":"263","author":"Akerman P","year":"1992","journal-title":"Am J Physiol"},{"key":"e_1_2_8_3_1","first-page":"397","article-title":"Cyclin D1 promotes mitogen\u2010independent cell cycle progression in hepatocytes","volume":"10","author":"Albrecht JH","year":"1999","journal-title":"Cell Growth Differ"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/path.2453"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2007.02.024"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.23059"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.21317"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M405703200"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjc.6606011"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/nbt1326"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1369\/0022155412438104"},{"key":"e_1_2_8_12_1","first-page":"1461","article-title":"Comparative electrophilicity, mutagenicity, DNA repair induction activity, and carcinogenicity of some N\u2010 and O\u2010acyl derivatives of N\u2010hydroxy\u20102\u2010aminoflourene","volume":"37","author":"Bartsch H","year":"1977","journal-title":"Cancer Res"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2008.06.001"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.120.3.757"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.21234"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V87.5.1851.1851"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.21183"},{"key":"e_1_2_8_18_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2004.11.006"},{"key":"e_1_2_8_19_1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.24507"},{"key":"e_1_2_8_20_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.132.6.1133"},{"key":"e_1_2_8_21_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrc1912"},{"key":"e_1_2_8_22_1","doi-asserted-by":"publisher","DOI":"10.1038\/labinvest.2008.71"},{"key":"e_1_2_8_23_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0403412101"},{"key":"e_1_2_8_24_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2667"},{"key":"e_1_2_8_25_1","first-page":"G387","article-title":"Mechanisms of hepatic toxicity. 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