ArticleJournal of endocrinological investigation2024
FBXO28 reduces high-fat diet-induced hyperlipidemia in mice by alleviating abnormal lipid metabolism and inflammatory responses.
Article in Journal of endocrinological investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Preclinical animal models of lower urinary tract dysfunction associated with metabolic syndrome.Nature reviews. Urology · 2026Review
- FBXO28 targets SNAI1 for ubiquitin-proteasomal degradation in non-small cell lung cancer.The Journal of biological chemistry · 2026Article
- Diagnostic and prognostic value of miR-885-5p in acute coronary syndrome and its regulatory mechanisms in endothelial injury.BMC cardiovascular disorders · 2026Article
- Anti-Metabolic Dysfunction-Associated Hepatic Steatosis Effects of Pickering Emulsion-Encapsulated Curcumin via Gut Microbiota and Short-Chain Fatty Acids Modulation in High-Fat-Diet Mice.Foods (Basel, Switzerland) · 2025Article
- Alleviating effect ofFrontiers in nutrition · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHyperlipidemia is a lipid metabolism disorder with increasing incidence and prevalence worldwide. Abnormal lipid metabolism and inflammation are two significant characteristics of hyperlipidemia. The purpose of this study was to explore the role and mechanism of F-box only protein 28 (FBXO28) in hyperlipidemia.
methodsMice were fed with high-fat diet (HFD) to elicit obesity, and 3T3-L1 preadipocytes were stimulated with MDI cocktail (IBMX, DEX and insulin) to evoke differentiation. In vivo and in vitro role of FBXO28 in hyperlipidemia was investigated by hematoxylin-eosin and oil Red O staining, the lipid biochemistry measurement, enzyme-linked immunosorbent assay, reverse transcription quantitative polymerase chain reaction and western blotting assays. The mechanism of FBXO28 explored by co-immunoprecipitation, immunofluorescence, ubiquitination and cycloheximide assays.
resultsLow expression of FBXO28 was found in hyperlipidemia in silico, in vivo and in vitro. Upregulation of FBXO28 declined the body weight, fat accumulation, and serum lipid content in HFD-fed mice. Abnormal lipid accumulation, and the level of liposynthetic genes and beta-oxidation related genes were improved by overexpression of FBXO28 both in HFD-elicited mice and MDI-treated 3T3-L1 preadipocytes. Besides, overexpression of FBXO28 declined HFD-induced the level of proinflammatory factors and F4/80. Mechanically, FBXO28 directly bound RAB27A and promoted its ubiquitinated degradation. Thus, upregulation of RAB27A inverted the improved role of FBXO28 in abnormal lipid metabolism and inflammation in vivo and in vitro.
conclusionFBXO28 ameliorated abnormal lipid metabolism and inflammation through the ubiquitinated degradation of RAB27A, thereby attenuating HFD-induced hyperlipidemia. The results could promote the treatment of hyperlipidemia, and the relevant diseases.
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