Abstract
Abnormal gene expression and secreted protein levels are accompanied by extensive pathological changes. Secreted frizzled related protein (SFRP) family members are antagonistic inhibitors of the Wnt signaling pathway, and they were recently found to be involved in the pathogenesis of a variety of metabolic diseases, which has led to extensive interest in SFRPs. Previous reports highlighted the importance of SFRPs in lipid metabolism, obesity, type 2 diabetes mellitus and cardiovascular diseases. In this review, we provide a detailed introduction of SFRPs, including their structural characteristics, receptors, inhibitors, signaling pathways and metabolic disease impacts. In addition to summarizing the pathologies and potential molecular mechanisms associated with SFRPs, this review further suggests the potential future use of SFRPs as disease biomarkers therapeutic targets.
Highlights
Metabolic syndrome (MetS) is a global epidemic that causes heavy social and economic burdens [1], and it consists of a group of cardiovascular risk factors, including dyslipidemia, glucose metabolism disorders, visceral obesity and hypertension [2]
We summarize the influence of Secreted frizzled related protein (SFRP) protein on physiological and pathological processes related to lipid metabolism and cardiovascular protection (Figures 3, 4)
Many important scientific problems have been solved since SFRPs proteins were first described, there are still many problems to be solved
Summary
Metabolic syndrome (MetS) is a global epidemic that causes heavy social and economic burdens [1], and it consists of a group of cardiovascular risk factors, including dyslipidemia, glucose metabolism disorders, visceral obesity and hypertension [2]. Overexpression of SFRP4 promoted human adipose tissue derived mesenchymal stem cells differentiation and lipid accumulation by antagonistic inhibition of the Wnt/b-catenin signaling pathway activated by Wnt3a [34]. The potential molecular mechanism involves GSK3 (an upstream regulator) activation of the signal transducer and activator of transcription 5 by phosphorylation, which binds and regulates the SFRP1 promoter, coordinately modulates adipogenic regulator expression and antagonizes canonical Wnt signaling induced adipogenesis [46] These results provide insights on the molecular mechanism of adipogenesis and provide an evidence that different adipogenic regulators coordinately modulate adipocyte differentiation. Activation of Wnt signaling via knockdown of SFRP4 inhibits adipogenesis while the treatment with SFRP4 induces a 1.5-fold increase in lipid accumulation in human adipose derived mesenchymal stem cells [34, 52], these findings demonstrate an interaction between Wnt antagonism and Wnt activation during adipogenesis. Compared with the healthy individuals, patients with polycystic ovary syndrome showed higher levels
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