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Retracted: Intestinal fatty acid‐binding protein mediates atherosclerotic progress through increasing intestinal inflammation and permeability
Author(s) -
Zhang Lulu,
Wang Fan,
Wang Jiajun,
Wang Yongshun,
Fang Yan
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15173
Subject(s) - intestinal permeability , inflammation , medicine , gene knockdown , endocrinology , immunology , biology , biochemistry , apoptosis
Atherosclerosis is one of leading phenotypes of cardiovascular diseases, featured with increased vascular intima‐media thickness (IMT) and unstable plaques. The interaction between gastrointestinal system and cardiovascular homeostasis is emerging as a hot topic. Therefore, the present study aimed to explore the role of an intestinal protein, intestinal fatty acid‐binding protein (I‐FABP/FABP2) in the atherosclerotic progress. In western diet–fed ApoE −/− mice, FABP2 was highly expressed in intestine. Silence of intestinal Fabp2 attenuated western diet–induced atherosclerotic phenotypes, including decreasing toxic lipid accumulation, vascular fibrosis and inflammatory response. Mechanistically, intestinal Fabp2 knockdown improved intestinal permeability through increasing the expression of tight junction proteins. Meanwhile, intestinal Fabp2 knockdown mice exhibited down‐regulation of intestinal inflammation in western diet–fed ApoE −/− mice. In clinical patients, the circulating level of FABP2 was obviously increased in patients with cardiovascular disease and positively correlated with the value of carotid intima‐media thickness, total cholesterol and triglyceride. In conclusion, FABP2‐induced intestinal permeability could address a potential role of gastrointestinal system in the development of atherosclerosis, and targeting on intestinal FABP2 might provide a therapeutic approach to protect against atherosclerosis.

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