Evidence map›Paper›PMID 42885393›Full record

ArticleAnimal models and experimental medicine2026

ABCA1 deficiency-induced cholesterol accumulation aggravates colonic epithelial injury in knockout hamsters.

Chang Liu, Jingjie Zheng, Sijing Shi, Jianwen Chen, Geroge Liu, Wei Huang, Xunde Xian, Yuhui Wang, Jianglin Fan, Ping Zhu and 1 more

Abstract read
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In one paragraph

Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Chang LiuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0009-0002-9771-2313
Jingjie ZhengGuangdong Province Key Laboratory of Large Animal Models for Biomedicine, South China Institute of Large Animal Models for Biomedicine, School of Pharmacy and Food Engineering, Wuyi University, Jiangmen, China.
Sijing ShiPeking University Institute of Cardiovascular Sciences, Beijing, China.
Jianwen ChenGuangdong Province Key Laboratory of Large Animal Models for Biomedicine, South China Institute of Large Animal Models for Biomedicine, School of Pharmacy and Food Engineering, Wuyi University, Jiangmen, China.
Geroge LiuPeking University Institute of Cardiovascular Sciences, Beijing, China.
Wei HuangPeking University Institute of Cardiovascular Sciences, Beijing, China.
Xunde XianPeking University Institute of Cardiovascular Sciences, Beijing, China.ORCID https://orcid.org/0000-0003-3059-1254
Yuhui WangPeking University Institute of Cardiovascular Sciences, Beijing, China.ORCID https://orcid.org/0000-0003-2936-3377
Jianglin FanGuangdong Province Key Laboratory of Large Animal Models for Biomedicine, South China Institute of Large Animal Models for Biomedicine, School of Pharmacy and Food Engineering, Wuyi University, Jiangmen, China.ORCID https://orcid.org/0000-0002-1737-6130
Ping ZhuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-4276-9593
Xiawen YangGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.ORCID https://orcid.org/0009-0008-3897-2610

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2025A1515012787Guangdong Major Project of Basic and Applied Basic Research 2023B0303000005
6 · The paper itself

Abstract

backgroundATP-binding cassette transporter A1 (ABCA1) mediates cellular cholesterol efflux, yet its role in inflammatory bowel disease (IBD) remains incompletely understood. This study investigated the consequences of intestinal epithelial cholesterol accumulation-primarily driven by ABCA1 deficiency-on colonic inflammation and the underlying molecular mechanisms.

methodsABCA1 knockout (KO) and wild-type (WT) Syrian golden hamsters were fed a high-cholesterol high-fat diet for 12 weeks. Colon specimens were analyzed for pathological changes, inflammatory markers, cholesterol accumulation, and gene expression profiles. Furthermore, in vitro experiments were performed using the human colon epithelial cell line Caco-2.

resultsABCA1 deficiency, in the context of a high-cholesterol high-fat diet, triggered significant colonic inflammation in KO hamsters, characterized by epithelial damage, inflammatory cell infiltration, and elevated pro-inflammatory cytokine levels. These pathological changes were associated with impaired mucosal barrier integrity, a four-fold increase in epithelial cholesterol accumulation, and reduced E-cadherin, ZO-1 and occludin expression. Furthermore, ABCA1 deficiency promoted oxidative stress and induced marked remodeling of the gut microbiota.

conclusionsOur findings establish a pathogenic role for ABCA1 deficiency in driving colonic epithelial injury and inflammation, suggesting that ABCA1 may play an important role in the pathogenesis of IBD.

Indexed as

ATP‐binding cassette transporter A1colonic epithelial cellsinflammatory bowel diseaseknockoutSyrian golden hamster

Identifiers

PMID42885393

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