Impact of intracellular glyceraldehyde-derived advanced glycation end-products on human hepatocyte cell death
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Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH); however, the pathogenesis of NASH currently remains unclear. We aimed to investigate the effects of intracellular glyceraldehyde (GA)-derived advanced glycation end-products (GA-AGEs) on human hepatocyte cell death. The accumulation of intracellular GA-AGEs has been associated with the induction of DNA damage and hepatocyte necrotic cell death. Among intracellular GA-AGEs, caspase-3 has been identified as a GA-AGE-modified protein with abrogated protein function. Furthermore, the activation of caspase-3 and induction of hepatocyte apoptosis by camptothecin, a DNA-damaging agent, was suppressed by a treatment with GA. These results suggest the inhibitory effects of GA-AGE-modified caspase-3 on the induction of DNA-damage-induced apoptosis, which is associated with hepatocyte necrosis. Therefore, the suppression of necrosis, the inflammatory form of cell death, by the accumulation of GA-AGEs and GA-AGE-modified caspase-3 may represent a novel therapeutic target for the pathogenesis of NASH.
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Intracellular AGE accumulation is observed in animal models of hepatic steatosis and other advanced liver diseases, such as steatohepatitis and fibrosis/cirrhosis.
“Intracellular AGE accumulation is observed in animal models of hepatic steatosis and other advanced liver diseases, such as hepatic inflammation (steatohepatitis) and fibrosis/cirrhosis.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [122]
Accumulated AGEs in hepatocytes stimulate apoptosis and inflammation, leading to cellular dysfunction, steatosis, and ultimately NAFLD.
“Accumulated AGEs in hepatocytes can stimulate apoptosis and inflammation, leading to cellular dysfunction, steatosis, and ultimately nonalcoholic fatty liver disease (NAFLD)121–123.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [122]
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Ikeda, T., Hong, S., Yoshida, S., Srivastava, S., Kunamneni, A., Yao, Y., Khuperkar, O., Basrur, V., Kuang, H., Kachman, M., et al. (2025) · bioRxiv · doi:10.1016/j.celrep.2025.116382 · Cited by 3 · see citing works
Brain angiopathy and impaired glucose metabolism in model mice with psychiatric-Related phenotypes
Hirai, S. (2020) · The Japanese Society for Neurochemistry
Okino, M., Yamashita, C., Takeuchi, M., Makino, R., & Tachibana, T. (2025) · Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology · doi:10.1016/j.cbpc.2025.110283
Self-citationThe Glycine-Proline-Hydroxyproline Tripeptide Reduces Cell Death Caused by Glycative Stress
Yamamoto, S., Matsumoto, Y., Yanbe, F., Sakai, A., Takeuchi, M., & Numata, N. (2026) · Protein and Peptide Letters · doi:10.2174/0109298665432008260403055737
Self-citationSakai, A., Takeda, K., & Takeuchi, M. (2026) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2026.154173
Self-citation
- Authors
- Sakasai-Sakai, A., Takata, T., Takino, J.-I., & Takeuchi, M.
- Affiliations
- Kanazawa Medical University (JP)
- Hiroshima International University (JP)
- Venue
- Scientific Reports
- Published
- 2017-10-27
- Volume
- 7
- Issue
- 1
- Pages
- 14282-14282
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5660208
- OpenAlex
- W2767048477
- Cited by
- 46
- References
- 53
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 6 · 2023: 10 · 2022: 2 · 2021: 4 · 2020: 8 · 2019: 5 · 2018: 1
- FWCI
- 3.18
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Japan Society for the Promotion of Science (15K16239, 26750056, 16H01811, 25282029)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- advanced glycation end products, glyceraldehyde, hepatocyte death, nonalcoholic steatohepatitis, caspase-3, DNA damage, apoptosis, liver necrosis, camptothecin, therapeutic target
- MeSH terms
- DNA Damage, Glyceraldehyde, Humans, Cell Death, Glycation End Products, Advanced, Protective Agents, Hepatocytes, Intracellular Space, Caspase 3, Hep G2 Cells, Non-alcoholic Fatty Liver Disease
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