The DOI matches its Crossref record; 218 of the 218 references it cites were found in a registry or an index.
Recent Insights into the Pathogenesis of Nonalcoholic Fatty Liver Disease
Open accessAbstract
Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem worldwide and an important risk factor for both hepatic and cardiometabolic mortality. The rapidly increasing prevalence of this disease and of its aggressive form nonalcoholic steatohepatitis (NASH) will require novel therapeutic approaches based on a profound understanding of its pathogenesis to halt disease progression to advanced fibrosis or cirrhosis and cancer. The pathogenesis of NAFLD involves a complex interaction among environmental factors (i.e., Western diet), obesity, changes in microbiota, and predisposing genetic variants resulting in a disturbed lipid homeostasis and an excessive accumulation of triglycerides and other lipid species in hepatocytes. Insulin resistance is a central mechanism that leads to lipotoxicity, endoplasmic reticulum stress, disturbed autophagy, and, ultimately, hepatocyte injury and death that triggers hepatic inflammation, hepatic stellate cell activation, and progressive fibrogenesis, thus driving disease progression. In the present review, we summarize the currently available data on the pathogenesis of NAFLD, emphasizing the most recent advances. A better understanding of NAFLD/NASH pathogenesis is crucial for the design of new and efficient therapeutic interventions.
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“BAs have emerged as important pathogenetic factors and therapeutic targets in both cholestatic and metabolic liver diseases.4 13 41”
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Cites
An obesity-associated gut microbiome with increased capacity for energy harvest
Turnbaugh, P. J., Ley, R. E., Mahowald, M. A., Magrini, V., Mardis, E. R., & Gordon, J. I. (2006) · Nature · doi:10.1038/nature05414 · Cited by 12,444
Pathogen Recognition and Innate Immunity
Akira, S., Uematsu, S., & Takeuchi, O. (2006) · Cell · doi:10.1016/j.cell.2006.02.015 · Cited by 12,401
Younossi, Z. M., Koenig, A. B., Abdelatif, D., Fazel, Y., Henry, L., & Wymer, M. (2016) · Hepatology · doi:10.1002/hep.28431 · Cited by 10,781
Pattern Recognition Receptors and Inflammation
Takeuchi, O., & Akira, S. (2010) · Cell · doi:10.1016/j.cell.2010.01.022 · Cited by 8,895
Yamauchi, T., Kamon, J., Waki, H., Terauchi, Y., Kubota, N., Hara, K., Mori, Y., Ide, T., Murakami, K., Tsuboyama-Kasaoka, N., et al. (2001) · Nature Medicine · doi:10.1038/90984 · Cited by 4,915
EASL–EASD–EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease
(2016) · Journal of Hepatology · doi:10.1016/j.jhep.2015.11.004 · Cited by 4,836
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
Duewell, P., Kono, H., Rayner, K. J., Sirois, C. M., Vladimer, G., Bauernfeind, F. G., Abela, G. S., Franchi, L., Nuñez, G., Schnurr, M., et al. (2010) · Nature · doi:10.1038/nature08938 · Cited by 4,026
Autophagy regulates lipid metabolism
Singh, R., Kaushik, S., Wang, Y., Xiang, Y., Novak, I., Komatsu, M., Tanaka, K., Cuervo, A. M., & Czaja, M. J. (2009) · Nature · doi:10.1038/nature07976 · Cited by 3,975
Chalasani, N., Younossi, Z. M., Lavine, J. E., Diehl, A. M., Brunt, E. M., Cusi, K. J., Charlton, M., & Sanyal, A. J. (2012) · Hepatology · doi:10.1002/hep.25762 · Cited by 3,859
Donnelly, K. L., Smith, C. I., Schwarzenberg, S. J., Jessurun, J., Boldt, M. D., & Parks, E. J. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23621 · Cited by 3,604
Research works printed but not linked: 6
- Arab JP, 2016, Ann. Hepatol., 15, 721
- Berlanga A, 2014, Clin. Exp. Gastroenterol., 7, 221
- 10.1002/cphy.c120035 · DOI · Paper page
- Mao J-W, 2015, Int. J. Clin. Exp. Pathol., 8, 3648
- de Mesquita FC, 2015, Hepatology, 62, 901A
- Loomba R, 2016, Hepatology, 64, 1119A
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Wang, X., He, Q., Zhou, C., Xu, Y., Liu, D., Fujiwara, N., Kubota, N., Click, A., Henderson, P., Vancil, J., et al. (2023) · Immunity · doi:10.1016/j.immuni.2022.11.013 · Cited by 262
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IL-6/STAT3 axis dictates the PNPLA3-mediated susceptibility to non-alcoholic fatty liver disease
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Song, K., Kwon, H., Han, C., Chen, W., Zhang, J., Ma, W., Dash, S., Gandhi, C. R., & Wu, T. (2020) · Hepatology · doi:10.1002/hep.30990 · Cited by 110
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Metadata
- Authors
- Arab, J. P., Arrese, M., & Trauner, M.
- Affiliations
- Mayo Clinic (US)
- Pontificia Universidad Católica de Chile (CL)
- Medical University of Vienna (AT)
- Corresponding author
- Trauner, Michael
- Venue
- Annual Review of Pathology Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2018-01-24
- Volume
- 13
- Issue
- 1
- Pages
- 321-350
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- OpenAlex
- W2785779482
- Cited by
- 573
- References
- 218
- Citations by year
- 2026: 43 · 2025: 64 · 2024: 76 · 2023: 85 · 2022: 61 · 2021: 93 · 2020: 77 · 2019: 47 · 2018: 26
- FWCI
- 8.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Association for the Study of Liver Diseases
- Vienna Science and Technology Fund
- Austrian Science Fund (F3008‐B19, F3517-B20, F3008, F3517)
- Fondo Nacional de Ciencia y Tecnología
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Keywords
- non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, pathogenesis, insulin resistance, lipotoxicity, endoplasmic reticulum stress, autophagy, liver inflammation, hepatic stellate cell activation, liver fibrosis, liver cirrhosis, hepatic lipid accumulation, gut microbiota, obesity, Western diet, genetic variants, cardiometabolic risk
- MeSH terms
- Animals, Humans, Non-alcoholic Fatty Liver Disease
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