The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Mechanisms of Disease Progression in Nonalcoholic Fatty Liver Disease
Abstract
Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of hepatic pathology, ranging from simple steatosis (also called nonalcoholic fatty liver or NAFL) in its most benign form, to cirrhosis in its most advanced form. Nonalcoholic steatohepatitis (NASH) is an intermediate level of hepatic pathology. Hepatocyte accumulation of triglyceride is a hallmark of NAFL and NASH, but this sometimes subsides once cirrhosis has developed. Triglyceride storage per se is not hepatotoxic. Rather, it is a marker of increased exposure of hepatocytes to potentially toxic fatty acids. NAFL progresses to NASH when adaptive mechanisms that protect hepatocytes from fatty acid-mediated lipotoxicity become overwhelmed and rates of hepatocyte death begin to outstrip mechanisms that normally regenerate dead hepatocytes. This triggers repair responses that involve activation of hepatic stellate cells to myofibroblasts. The myofibroblasts generate excessive matrix and produce factors that stimulate expansion of liver progenitor populations. The progenitor cells produce chemokines to attract various kinds of inflammatory cells to the liver. They also differentiate to replace the dead hepatocytes. The intensity of these repair responses generally parallel the degree of hepatocyte death, resulting in variable distortion of the hepatic architecture with fibrosis, infiltrating immune cells, and regenerating epithelial nodules. As in other types of chronic liver injury, cirrhosis ensues in patients with NAFLD when repair is extreme and sustained, but ultimately unsuccessful, at reconstituting healthy hepatic epithelia.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Xu, H., Barnes, G. T., Yang, Q., Tan, G., Yang, D., Chou, C. J., Sole, J., Nichols, A., Ross, J. S., Tartaglia, L. A., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200319451 · Cited by 6,760
Nonalcoholic Fatty Liver Disease
Angulo, P. (2002) · New England Journal of Medicine · doi:10.1056/nejmra011775 · Cited by 5,228
Steatohepatitis: A tale of two “hits”?
Day, C. P., & James, O. F. W. (1998) · Gastroenterology · doi:10.1016/s0016-5085(98)70599-2 · Cited by 4,285
Local and systemic insulin resistance resulting from hepatic activation of IKK-β and NF-κB
Cai, D., Yuan, M., Frantz, D. F., Melendez, P. A., Hansen, L., Lee, J., & Shoelson, S. E. (2005) · Nature Medicine · doi:10.1038/nm1166 · Cited by 2,245
Xu, A., Wang, Y., Keshaw, H., Xu, L. Y., Lam, K. S. L., & Cooper, G. J. S. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200317797 · Cited by 1,298
Beyond insulin resistance in NASH: TNF-α or adiponectin?
Hui, J. M., Hodge, A., Farrell, G. C., Kench, J. G., Kriketos, A., & George, J. (2004) · Hepatology · doi:10.1002/hep.20280 · Cited by 942
Hotamisligil, G. S., Budavari, A., Murray, D., & Spiegelman, B. M. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117495 · Cited by 819
Cloning of DGAT2, a Second Mammalian Diacylglycerol Acyltransferase, and Related Family Members
Cases, S., Stone, S. J., Zhou, P., Yen, E., Tow, B., Lardizabal, K. D., Voelker, T., & Farese, R. V. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m106219200 · Cited by 818
Choi, C. S., Savage, D. B., Kulkarni, A., Yu, X. X., Liu, Z.-X., Morino, K., Kim, S., Distefano, A., Samuel, V. T., Neschen, S., et al. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m704213200 · Cited by 383
Zhan, S.-S., Jiang, J. X., Wu, J., Halsted, C., Friedman, S. L., Zern, M. A., & Torok, N. J. (2006) · Hepatology · doi:10.1002/hep.21093 · Cited by 284
Cited by
Neuschwander‐Tetri, B. A. (2010) · Hepatology · doi:10.1002/hep.23719 · Cited by 1,077
Nonalcoholic Fatty Liver Disease: Pathology and Pathogenesis
Tiniakos, D. G., Vos, M. B., & Brunt, E. M. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102132 · Cited by 870
Stienstra, R., Saudale, F., Duval, C., Keshtkar, S., Groener, J. E. M., van Rooijen, N., Staels, B., Kersten, S., & Müller, M. (2010) · Hepatology · doi:10.1002/hep.23337 · Cited by 452
Speliotes, E. K., Butler, J. L., Palmer, C. D., Voight, B. F., & Hirschhorn, J. N. (2010) · Hepatology · doi:10.1002/hep.23768 · Cited by 362
Jiang, J. X., Chen, X., Serizawa, N., Szyndralewiez, C., Page, P., Schröder, K., Brandes, R. P., Devaraj, S., & Török, N. J. (2012) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2012.05.007 · Cited by 251
Nonalcoholic fatty liver disease
Erickson, S. K. (2009) · Journal of Lipid Research · doi:10.1194/jlr.r800089-jlr200 · Cited by 194
Quantification and mechanisms of oleic acid-induced steatosis in HepG2 cells.
(2010) · PubMed Central · Cited by 181
Bettaieb, A., Jiang, J. X., Sasaki, Y., Chao, T.-I., Kiss, Z., Chen, X., Tian, J., Katsuyama, M., Yabe-Nishimura, C., Xi, Y., et al. (2015) · Gastroenterology · doi:10.1053/j.gastro.2015.04.009 · Cited by 167
Pathogenesis of alcohol‐induced liver disease: Classical concepts and recent advances
Seth, D., Haber, P. S., Syn, W., Diehl, A. M., & Day, C. P. (2011) · Journal of Gastroenterology and Hepatology · doi:10.1111/j.1440-1746.2011.06756.x · Cited by 166
Self-citationGan, L., Chitturi, S., & Farrell, G. C. (2011) · Current Gerontology and Geriatrics Research · doi:10.1155/2011/831536 · Cited by 135
Non-alcoholic Fatty Liver Disease and Alcohol-Related Liver Disease: Two Intertwined Entities
Idalsoaga, F., Kulkarni, A. V., Mousa, O. Y., Arrese, M., & Arab, J. P. (2020) · Frontiers in Medicine · doi:10.3389/fmed.2020.00448 · Cited by 136
Interactions between hepatic iron and lipid metabolism with possible relevance to steatohepatitis
Ahmed, U. (2012) · World Journal of Gastroenterology · doi:10.3748/wjg.v18.i34.4651 · Cited by 121
Fatty Acids - Induced Lipotoxicity and Inflammation
Savary, S., Trompier, D., Andreoletti, P., Le Borgne, F., Demarquoy, J., & Lizard, G. (2012) · Current Drug Metabolism · doi:10.2174/138920012803762729 · Cited by 111
Short-term exercise reduces markers of hepatocyte apoptosis in nonalcoholic fatty liver disease
Fealy, C. E., Haus, J. M., Solomon, T. P. J., Pagadala, M., Flask, C. A., McCullough, A. J., & Kirwan, J. P. (2012) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00127.2012 · Cited by 102
Yin, X., Zheng, F., Pan, Q., Zhang, S., Yu, D., Xu, Z., & Li, H. (2015) · Journal of Molecular Endocrinology · doi:10.1530/jme-15-0101 · Cited by 67
Promrat, K., Longato, L., Wands, J. R., & de la Monte, S. M. (2011) · Hepatology Research · doi:10.1111/j.1872-034x.2011.00815.x · Cited by 66
Johnson, N. D., Wu, X., Still, C. D., Chu, X., Petrick, A. T., Gerhard, G. S., Conneely, K. N., & DiStefano, J. K. (2021) · Clinical Epigenetics · doi:10.1186/s13148-021-01129-y · Cited by 43
Chiba, M., Sasaki, M., Kitamura, S., Ikeda, H., Sato, Y., & Nakanuma, Y. (2011) · Journal of Clinical Pathology · doi:10.1136/jcp.2011.090175 · Cited by 43
Metadata
- Authors
- Jou, J., Choi, S., & Diehl, A.
- Venue
- Seminars in Liver Disease
- Publisher
- Georg Thieme Verlag KG
- Published
- 2008-10-27
- Volume
- 28
- Issue
- 04
- Pages
- 370-379
- ISSN
- 0272-8087 (ISSN-L)
- 1098-8971
- OpenAlex
- W2019048359
- Cited by
- 482
- References
- 12
- FWCI
- 24.75
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
