title: Bile acid signaling and liver regeneration.
abstract: The liver is able to regenerate itself in response to partial hepatectomy or liver injury. This is accomplished by a complex network of different cell types and signals both inside and outside the liver. Bile acids (BAs) are recently identified as liver-specific metabolic signals and promote liver regeneration by activating their receptors: Farnesoid X Receptor (FXR) and G-protein-coupled BA receptor 1 (GPBAR1, or TGR5). FXR is a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors. FXR promotes liver regeneration after 70% partial hepatectomy (PHx) or liver injury. Moreover, activation of FXR is able to alleviate age-related liver regeneration defects. Both liver- and intestine-FXR are activated by BAs after liver resection or injury and promote liver regeneration through distinct mechanism. TGR5 is a membrane-bound BA receptor and it is also activated during liver regeneration. TGR5 regulates BA hydrophobicity and stimulates BA excretion in urine during liver regeneration. BA signaling thus represents a novel metabolic pathway during liver regeneration. This article is part of a Special Issue entitled: Nuclear receptors in animal development.
authors.affiliation: Institute of Genetics, College of Life Science, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
authors.forename: Mingjie
authors.initials: M
authors.lastname: Fan
authors.affiliation: Department of Diabetes and Metabolic Diseases Research, Beckman Research Institute, City of Hope National Medical Center, 1500 E. Duarte Road, Duarte, CA 91010, USA.
authors.forename: Xichun
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Diabetes and Metabolic Diseases Research, Beckman Research Institute, City of Hope National Medical Center, 1500 E. Duarte Road, Duarte, CA 91010, USA.
authors.forename: Ganyu
authors.initials: G
authors.lastname: Xu
authors.affiliation: Institute of Genetics, College of Life Science, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
authors.forename: Qingfeng
authors.initials: Q
authors.lastname: Yan
authors.affiliation: Institute of Genetics, College of Life Science, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China; Department of Diabetes and Metabolic Diseases Research, Beckman Research Institute, City of Hope National Medical Center, 1500 E. Duarte Road, Duarte, CA 91010, USA. Electronic address: whuang@coh.org.
authors.forename: Wendong
authors.initials: W
authors.lastname: Huang
mesh_terms: D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000502:physiology*; D008115:Liver Regeneration; D018160:Receptors, Cytoplasmic and Nuclear / Q000502:physiology; D043562:Receptors, G-Protein-Coupled / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics; D000099150:Receptor, Farnesoid X-Activated
chemical_list: D001647:Bile Acids and Salts; D018160:Receptors, Cytoplasmic and Nuclear; D043562:Receptors, G-Protein-Coupled; D000099150:Receptor, Farnesoid X-Activated; C473772:GPBAR1 protein, human
keywords: Bile acid; FGF15; FXR; Liver regeneration; TGR5