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        <identifier>oai:figshare.com:article/34029462</identifier>
        <datestamp>2026-09-30T04:24:29Z</datestamp>
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          <dc:title>Presentation 1_Apelin aggravates inflammatory response and hepatic steatosis in alcohol-associated liver disease via ERK signaling pathway.pptx</dc:title>
          <dc:creator>Hongyan Bian (19186106)</dc:creator>
          <dc:creator>Aochun Wu (25141281)</dc:creator>
          <dc:creator>Jinlin Tang (23760725)</dc:creator>
          <dc:creator>Zhiwei Wang (120259)</dc:creator>
          <dc:creator>Jiayi Song (3936518)</dc:creator>
          <dc:creator>Yi Meng (2655814)</dc:creator>
          <dc:creator>Xiao Xu (112147)</dc:creator>
          <dc:creator>Xinrui Lv (4841010)</dc:creator>
          <dc:subject>Pharmacology</dc:subject>
          <dc:subject>alcoholic liver disease</dc:subject>
          <dc:subject>apelin</dc:subject>
          <dc:subject>APJ</dc:subject>
          <dc:subject>ERK</dc:subject>
          <dc:subject>hepatic Kupffer cell</dc:subject>
          <dc:description>Background&lt;p&gt;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.&lt;/p&gt;Methods&lt;p&gt;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&amp;E and Oil Red O staining.&lt;/p&gt;Results&lt;p&gt;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.&lt;/p&gt;Conclusion&lt;p&gt;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.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-30T04:24:29Z</dc:date>
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          <dc:identifier>10.3389/fphar.2026.1912482.s001</dc:identifier>
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          <dc:rights>CC BY 4.0</dc:rights>
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