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Peer-reviewedCC BYFrontiers in pharmacology

Apelin aggravates inflammatory response and hepatic steatosis in alcohol-associated liver disease via ERK signaling pathway

  • Hongyan Bian1
  • Aochun Wu1
  • Jinlin Tang1
  • Zhiwei Wang1
  • Jiayi Song1
  • Yi Meng1
  • Xiao Xu1
  • Xinrui Lv1
  1. 1Kaifeng Key Laboratory for Infectious Diseases and Biosafety , ,
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Abstract

Background: Though apelin is involved in cardiovascular, metabolic, and homeostasis disorders, its role in alcohol-associated liver disease (ALD) remains unclear. This study aimed to investigate the mechanism of apelin in promoting hepatic inflammation in ALD.

Methods: RAW 264.7 macrophages and a chronic alcohol-fed C57BL/6 mouse model were used. Apelin activated ERK1/2 phosphorylation, and PD98059 pretreatment attenuated apelin-induced MCP-1 and PCNA expression. Inflammatory and proliferative markers (MCP-1, IL-6, PCNA) were assessed by qRT-PCR and western blot. ERK signaling was evaluated using the inhibitor PD98059. Liver pathology was examined by H&E and Oil Red O staining.

Results: Alcohol upregulated apelin expression in RAW 264.7 cells. Apelin-13 increased MCP-1 and PCNA expression in time- and dose-dependent manners. Apelin overexpression enhanced, while siRNA knockdown reduced, inflammatory and proliferative gene expression. Apelin activated ERK1/2 phosphorylation, and PD98059 pretreatment attenuated apelin-induced MCP-1 and PCNA expression. In vivo , apelin overexpression exacerbated steatosis, ballooning degeneration, and inflammatory infiltration, with elevated MCP-1, IL-6, and PCNA levels.

Conclusion: Apelin aggravates inflammatory responses and hepatic steatosis in ALD via the ERK signaling pathway, suggesting that the apelin/APJ/p-ERK/inflammation axis may represent a novel therapeutic target for ALD.

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Cite

BibTeXRIS
BibTeX
@article{bian2026apelin,
  title = {{Apelin aggravates inflammatory response and hepatic steatosis in alcohol-associated liver disease via ERK signaling pathway}},
  author = {Hongyan Bian and Aochun Wu and Jinlin Tang and Zhiwei Wang and Jiayi Song and Yi Meng and Xiao Xu and Xinrui Lv},
  journal = {Frontiers in pharmacology},
  year = {2026},
  month = sep,
  doi = {10.3389/fphar.2026.1912482},
  url = {https://europepmc.org/article/PMC/PMC13661315},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Apelin aggravates inflammatory response and hepatic steatosis in alcohol-associated liver disease via ERK signaling pathway
AU  - Hongyan Bian
AU  - Aochun Wu
AU  - Jinlin Tang
AU  - Zhiwei Wang
AU  - Jiayi Song
AU  - Yi Meng
AU  - Xiao Xu
AU  - Xinrui Lv
PY  - 2026
DA  - 2026/09/30
JO  - Frontiers in pharmacology
DO  - 10.3389/fphar.2026.1912482
UR  - https://europepmc.org/article/PMC/PMC13661315
AB  - Background: Though apelin is involved in cardiovascular, metabolic, and homeostasis disorders, its role in alcohol-associated liver disease (ALD) remains unclear. This study aimed to investigate the mechanism of apelin in promoting hepatic inflammation in ALD.  Methods: RAW 264.7 macrophages and a chronic alcohol-fed C57BL/6 mouse model were used. Apelin activated ERK1/2 phosphorylation, and PD98059 pretreatment attenuated apelin-induced MCP-1 and PCNA expression. Inflammatory and proliferative markers (MCP-1, IL-6, PCNA) were assessed by qRT-PCR and western blot. ERK signaling was evaluated using the inhibitor PD98059. Liver pathology was examined by H&E and Oil Red O staining.  Results: Alcohol upregulated apelin expression in RAW 264.7 cells. Apelin-13 increased MCP-1 and PCNA expression in time- and dose-dependent manners. Apelin overexpression enhanced, while siRNA knockdown reduced, inflammatory and proliferative gene expression. Apelin activated ERK1/2 phosphorylation, and PD98059 pretreatment attenuated apelin-induced MCP-1 and PCNA expression. In vivo , apelin overexpression exacerbated steatosis, ballooning degeneration, and inflammatory infiltration, with elevated MCP-1, IL-6, and PCNA levels.  Conclusion: Apelin aggravates inflammatory responses and hepatic steatosis in ALD via the ERK signaling pathway, suggesting that the apelin/APJ/p-ERK/inflammation axis may represent a novel therapeutic target for ALD.
SN  - 1663-9812
ER  -