The DOI matches its Crossref record; 214 of the 214 references it cites were found in a registry or an index.
Molecular Mechanisms of Alcoholic Fatty Liver
Open accessAbstract
Alcoholic fatty liver is a potentially pathologic condition which can progress to steatohepatitis, fibrosis, and cirrhosis if alcohol consumption is continued. Alcohol exposure may induce fatty liver by increasing NADH/NAD+ratio, increasing sterol regulatory element‐binding protein‐1 (SREBP‐1) activity, decreasing peroxisome proliferator‐activated receptor‐α (PPAR‐α) activity, and increasing complement C3 hepatic levels. Alcohol may increase SREBP‐1 activity by decreasing the activities of AMP‐activated protein kinase and sirtuin‐1. Tumor necrosis factor‐α (TNF‐α) produced in response to alcohol exposure may cause fatty liver by up‐regulating SREBP‐1 activity, whereas betaine and pioglitazone may attenuate fatty liver by down‐regulating SREBP‐1 activity. PPAR‐α agonists have potentials to attenuate alcoholic fatty liver. Adiponectin and interleukin‐6 may attenuate alcoholic fatty liver by up‐regulating PPAR‐α and insulin signaling pathways while down‐regulating SREBP‐1 activity and suppressing TNF‐α production. Recent studies show that paracrine activation of hepatic cannabinoid receptor 1 by hepatic stellate cell‐derived endocannabinoids also contributes to the development of alcoholic fatty liver. Furthermore, oxidative modifications and inactivation of the enzymes involved in the mitochondrial and/or peroxisomal β‐oxidation of fatty acids could contribute to fat accumulation in the liver.
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“Ethanol metabolism primarily occurs in the liver in three major steps: (1) ethanol oxidation to acetaldehyde, (2) acetaldehyde metabolism to acetate, and (3) acetate catabolism to H2O and CO2132–134.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
In the citing paper
“Cytosolic ADH is a major enzyme that catalyzes the oxidative metabolism of ethanol to acetaldehyde by using the cofactor nicotinamide adenine dinucleotide (NAD+) converted to NADH132–134.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
In the citing paper
“Catalase present in peroxisomes may participate in ethanol oxidation in the presence of H2O2132–134, although this enzyme appears to play no major role in hepatic ethanol metabolism under physiological conditions due to the limited supply of H2O2135.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
In the citing paper
“Finally, the acetate that is produced is further degraded to CO2 and H2O, ending the final step of ethanol oxidation in the liver132–134.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [132]
In the citing paper
“Continued mitochondrial dysfunction with increased oxidative stress also sensitizes the hepatocytes to subsequent necrosis and/or apoptosis of hepatocytes, which likely lead to activation of resident liver macrophage (i.e., Kupffer cells) and recruitment of infiltrating immune cells into the liver with elevated levels of hepatic inflammation (steatohepatitis) and pro-inflammatory cytokines/chemok”
In the citing paper
“Inactivation of AMPK is known to be associated with AFLD and NAFLD or acute liver injury, as reviewed [13].”
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Citations
Cites
Items 201–214 of 214
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Research works printed but not linked: 1
- 10.1172/JCI200523057 · DOI
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Seitz, H. K., Bataller, R., Cortez-Pinto, H., Gao, B., Gual, A., Lackner, C., Mathurin, P., Mueller, S., Szabo, G., & Tsukamoto, H. (2018) · Nature Reviews Disease Primers · doi:10.1038/s41572-018-0014-7 · Cited by 1,271
Self-citationRungratanawanich, W., Qu, Y., Wang, X., Essa, M. M., & Song, B.-J. (2021) · Experimental & Molecular Medicine · doi:10.1038/s12276-021-00561-7 · Cited by 411
Self-citationLeFort, K. R., Rungratanawanich, W., & Song, B.-J. (2024) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-05061-7 · Cited by 202
Self-citationCYP2E1 potentiates binge alcohol-induced gut leakiness, steatohepatitis, and apoptosis
Abdelmegeed, M. A., Banerjee, A., Jang, S., Yoo, S.-H., Yun, J.-W., Gonzalez, F. J., Keshavarzian, A., & Song, B.-J. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.09.009 · Cited by 191
Self-citationSong, B.-J., Akbar, M., Abdelmegeed, M. A., Byun, K., Lee, B., Yoon, S. K., & Hardwick, J. P. (2014) · Redox Biology · doi:10.1016/j.redox.2014.10.004 · Cited by 123
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Metadata
- Authors
- Purohit, V., Gao, B., & Song, B.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Purohit, Vishnudutt
- Venue
- Alcoholism: Clinical and Experimental Research
- Publisher
- Wiley
- Published
- 2009-01-22
- Volume
- 33
- Issue
- 2
- Pages
- 191-205
- ISSN
- 0145-6008 (ISSN-L)
- 1530-0277
- PMC
- PMC2633431
- OpenAlex
- W2066238144
- Cited by
- 312
- References
- 214
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 18 · 2023: 18 · 2022: 12 · 2021: 16 · 2020: 17 · 2019: 20 · 2018: 14 · 2017: 20 · 2016: 17 · 2015: 24 · 2014: 26 · 2013: 16 · 2012: 28
- FWCI
- 2.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Alcoholism Clinical and Experimental Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99‐AA999999, Z99 DA999999)
- National Institute on Alcohol Abuse and Alcoholism (Z01AA000036)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- alcoholic fatty liver, steatohepatitis, liver fibrosis, liver cirrhosis, SREBP1, PPARα, NAD+/NADH ratio, AMPK, SIRT1, TNF-α, complement C3, betaine, pioglitazone, adiponectin, interleukin-6, insulin signaling, hepatic stellate cells, CB1 receptor, endocannabinoids, fatty acid beta-oxidation, oxidative modification, hepatic lipid accumulation
- MeSH terms
- Animals, Complement C3, Fatty Liver, Alcoholic, Humans, NAD, Tumor Necrosis Factor-alpha, PPAR alpha, Sterol Regulatory Element Binding Proteins
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