Metabolic injury of hepatocytes promotes progression of NAFLD and AALD
Open accessAbstract
Nonalcoholic liver disease is a component of metabolic syndrome associated with obesity, insulin resistance, and hyperlipidemia. Excessive alcohol consumption may accelerate the progression of steatosis, steatohepatitis, and fibrosis. While simple steatosis is considered a benign condition, nonalcoholic steatohepatitis with inflammation and fibrosis may progress to cirrhosis, liver failure, and hepatocellular cancer. Studies in rodent experimental models and primary cell cultures have demonstrated several common cellular and molecular mechanisms in the pathogenesis and regression of liver fibrosis. Chronic injury and death of hepatocytes cause the recruitment of myeloid cells, secretion of inflammatory and fibrogenic cytokines, and activation of myofibroblasts, resulting in liver fibrosis. In this review, we discuss the role of metabolically injured hepatocytes in the pathogenesis of nonalcoholic steatohepatitis and alcohol-associated liver disease. Specifically, the role of chemokine production and de novo lipogenesis in the development of steatotic hepatocytes and the pathways of steatosis regulation are discussed.
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Key responses of hepatocytes to metabolic injury include activation of inflammatory and pro-apoptotic signalling via TNFα and NF-κB, favouring hepatocyte cell death pathways and/or senescence.
“Key responses of hepatocytes to metabolic injury include the activation of inflammatory and pro-apoptotic signalling, e.g. via tumour necrosis factor (TNF)α and NF-κB,3 favouring hepatocyte cell death pathways and/or senescence.16,17”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [16]
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References 185 · Cited by 23
- Authors
- Carvalho-Gontijo, R., Han, C., Zhang, L., Zhang, V., Hosseini, M., Mekeel, K., Schnabl, B., Loomba, R., Karin, M., Brenner, D. A., & Kisseleva, T.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Kisseleva, Tatiana
- ORCID
- Venue
- Seminars in Liver Disease
- Publisher
- Georg Thieme Verlag KG
- Published
- 2022-08
- Volume
- 42
- Issue
- 03
- Pages
- 233-249
- ISSN
- 0272-8087 (ISSN-L)
- 1098-8971
- PMC
- PMC9662188
- OpenAlex
- W4293105615
- Cited by
- 23
- References
- 185
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 5 · 2023: 6 · 2022: 2
- FWCI
- 0.75
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Liver Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (UL1TR001442)
- National Institute on Alcohol Abuse and Alcoholism (U01AA026939, U01AA029019, U01AA022614, U01AA018663, R01AA024726, R01AA028550, P50AA011999, R37AA020703)
- National Heart, Lung, and Blood Institute (P01HL147835)
- National Cancer Institute (R01CA234128)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK124318, R01DK111866, R44DK115242, R01DK121378, R01DK106419, F32DK009920, P30DK120515, R01DK101737, U01DK061734, R01DK091183, R01DK099205)
- National Institute of Environmental Health Sciences (P42ES010337)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Epidemiology › 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
- nonalcoholic steatohepatitis, alcoholic liver disease, liver fibrosis, steatosis, de novo lipogenesis, chemokines, myofibroblast activation, myeloid cell recruitment, fibrogenic cytokines, liver cirrhosis, non-alcoholic fatty liver disease
- MeSH terms
- Humans, Insulin Resistance, Liver, Liver Cirrhosis, Obesity, Hepatocytes, Non-alcoholic Fatty Liver Disease
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