The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Role of Nuclear Receptors in the Adaptive Response to Bile Acids and Cholestasis: Pathogenetic and Therapeutic Considerations
Abstract
Cholestasis results in intrahepatic accumulation of cytotoxic bile acids which cause liver injury ultimately leading to biliary fibrosis and cirrhosis. Cholestatic liver damage is counteracted by a variety of intrinsic hepatoprotective mechanisms. Such defense mechanisms include repression of hepatic bile acid uptake and de novo bile acid synthesis. Furthermore, phase I and II bile acid detoxification is induced rendering bile acids more hydrophilic. In addition to "orthograde" export via canalicular export systems, these compounds are also excreted via basolateral "alternative" export systems into the systemic circulation followed by renal elimination. Passive glomerular filtration of hydrophilic bile acids, active renal tubular secretion, and repression of tubular bile acid reabsorption facilitate renal bile acid elimination during cholestasis. The underlying molecular mechanisms are mediated mainly at a transcriptional level via a complex network involving nuclear receptors and other transcription factors. So far, the farnesoid X receptor FXR, pregnane X receptor PXR, and vitamin D receptor VDR have been identified as nuclear receptors for bile acids. However, the intrinsic adaptive response to bile acids cannot fully prevent liver injury in cholestasis. Therefore, additional therapeutic strategies such as targeted activation of nuclear receptors are needed to enhance the hepatic defense against toxic bile acids.
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Citations
Cites
The coregulator exchange in transcriptional functions of nuclear receptors
Glass, C. K., & Rosenfeld, M. G. (2000) · Genes & Development · doi:10.1101/gad.14.2.121 · Cited by 2,233
Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis
Inagaki, T., Choi, M., Moschetta, A., Peng, L., Cummins, C. L., McDonald, J. G., Luo, G., Jones, S. A., Goodwin, B., Richardson, J. A., et al. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2005.09.001 · Cited by 1,865
The PPARs: From Orphan Receptors to Drug Discovery
Willson, T. M., Brown, P. J., Sternbach, D. D., & Henke, B. R. (2000) · Journal of Medicinal Chemistry · doi:10.1021/jm990554g · Cited by 1,816
Endogenous Bile Acids Are Ligands for the Nuclear Receptor FXR/BAR
Wang, H., Chen, J., Hollister, K., Sowers, L. C., & Forman, B. M. (1999) · Molecular Cell · doi:10.1016/s1097-2765(00)80348-2 · Cited by 1,636
Vitamin D Receptor As an Intestinal Bile Acid Sensor
Makishima, M., Lu, T. T., Xie, W., Whitfield, G. K., Domoto, H., Evans, R. M., Haussler, M. R., & Mangelsdorf, D. J. (2002) · Science · doi:10.1126/science.1070477 · Cited by 1,176
Bile salt transporters: molecular characterization, function, and regulation
Trauner, M., & Boyer, J. L. (2003) · Physiological Reviews · doi:10.1152/physrev.00027.2002 · Cited by 999
Self-citationPaumgartner, G., & Beuers, U. (2002) · Hepatology · doi:10.1053/jhep.2002.36088 · Cited by 748
Pellicciari, R., Fiorucci, S., Camaioni, E., Clerici, C., Costantino, G., Maloney, P. R., Morelli, A., Parks, D. J., & Willson, T. M. (2002) · Journal of Medicinal Chemistry · doi:10.1021/jm025529g · Cited by 743
Wagner, M., Halilbasic, E., Marschall, H., Zollner, G., Fickert, P., Langner, C., Zatloukal, K., Denk, H., & Trauner, M. (2005) · Hepatology · doi:10.1002/hep.20784 · Cited by 355
Self-citationTreatment of pruritus of primary biliary cirrhosis with rifampin
Podesta, A., Lopez, P., Terg, R., Villamil, F., Flores, D., Mastai, R., Udaondo, C. B., & Companc, J. P. (1991) · Digestive Diseases and Sciences · doi:10.1007/bf01300759 · Cited by 267
Coordinate transcriptional regulation of bile acid homeostasis and drug metabolism
Eloranta, J. J., & Kullak-Ublick, G. A. (2005) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2004.09.019 · Cited by 260
Effects of long-term rifampicin administration in primary biliary cirrhosis
Bachs, L., Parés, A., Elena, M., Piera, C., & Rodés, J. (1992) · Gastroenterology · doi:10.1016/0016-5085(92)90335-v · Cited by 235
Phenobarbital Effects in Cholestatic Liver Disease
BLOOMER, J. R., & BOYER, J. L. (1975) · Annals of Internal Medicine · doi:10.7326/0003-4819-82-3-310 · Cited by 120
Cited by
Bile acid-microbiota crosstalk in gastrointestinal inflammation and carcinogenesis
Jia, W., Xie, G., & Jia, W. (2018) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2017.119 · Cited by 1,924
Role of Bile Acids and Bile Acid Receptors in Metabolic Regulation
Lefebvre, P., Cariou, B., Lien, F., Kuipers, F., & Staels, B. (2009) · Physiological Reviews · doi:10.1152/physrev.00010.2008 · Cited by 1,678
Bile acids: regulation of synthesis
Chiang, J. Y. L. (2009) · Journal of Lipid Research · doi:10.1194/jlr.r900010-jlr200 · Cited by 1,515
Targeting bile‐acid signalling for metabolic diseases
Thomas, C., Pellicciari, R., Pruzanski, M., Auwerx, J., & Schoonjans, K. (2008) · Nature Reviews Drug Discovery · doi:10.1038/nrd2619 · Cited by 1,422
Systemic gut microbial modulation of bile acid metabolism in host tissue compartments
Swann, J. R., Want, E. J., Geier, F. M., Spagou, K., Wilson, I. D., Sidaway, J. E., Nicholson, J. K., & Holmes, E. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1006734107 · Cited by 726
Metadata
- Authors
- Zollner, G., Marschall, H.-U., Wagner, M., & Trauner, M.
- Venue
- Molecular Pharmaceutics
- Publisher
- American Chemical Society (ACS)
- Published
- 2006-05-19
- Volume
- 3
- Issue
- 3
- Pages
- 231-251
- ISSN
- 1543-8384 (ISSN-L)
- 1543-8392
- OpenAlex
- W1966514588
- Cited by
- 335
- References
- 13
- FWCI
- 15.50
- Type
- journal article
- Language
- en
- Open access
- closed
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