Corrigendum to “Facilitatory effects of fetuin-A on atherosclerosis” [Atherosclerosis 246 (2016) 344–351]

Naito, C; H, Mio; Watanabe, K.; Shirai, Ryuichi; Takahashi, Yasuhiro; Kojima, Miho; Watanabe, Ryoji; Sato, Kengo; Iso, Yoshitaka; Matsuyama, Taka‐aki; Suzuki, Hiroshi; Ishibashi‐Ueda, Hatsue; Watanabe, Takuya

doi:10.1016/j.atherosclerosis.2016.05.009

Cited by 2 publications

(1 citation statement)

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“…In addition to its adverse effects on insulin resistance, fetuin-A has been correlated with other metabolic diseases 42 , 43 . von Loeffelholz et al showed that compared to patients with non-nonalcoholic fatty liver disease (non-NAFLD), circulating levels of fetuin-A were increased in patients with NAFLD, and Naito et al reported that fetuin-A induced endothelial dysfunction and promoted macrophage foam cell formation, leading to the progression of atherosclerosis 42 , 43 . Apigenin has been reported to be beneficial for the treatment of metabolic diseases, including obesity, NAFLD, and atherosclerosis 22 , 44 .…”

Section: Discussionmentioning

confidence: 99%

Apigenin targets fetuin-A to ameliorate obesity-induced insulin resistance

Hsu,

Chen,

Wang

et al. 2024

Int. J. Biol. Sci.

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Fetuin-A, a hepatokine secreted by hepatocytes, binds to insulin receptors and consequently impairs the activation of the insulin signaling pathway, leading to insulin resistance. Apigenin, a flavonoid isolated from plants, has beneficial effects on insulin resistance; however, its regulatory mechanisms are not fully understood. In the present study, we investigated the molecular mechanisms underlying the protective effects of apigenin on insulin resistance. In Huh7 cells, treatment with apigenin decreased the mRNA expression of fetuin-A by decreasing reactive oxygen species-mediated casein kinase 2α (CK2α)-nuclear factor kappa-light-chain-enhancer of activated B activation; besides, apigenin decreased the levels of CK2α-dependent fetuin-A phosphorylation and thus promoted fetuin-A degradation through the autophagic pathway, resulting in a decrease in the protein levels of fetuin-A. Moreover, apigenin prevented the formation of the fetuin-A-insulin receptor (IR) complex and thereby rescued the PA-induced impairment of the insulin signaling pathway, as evidenced by increased phosphorylation of IR substrate-1 and Akt, and translocation of glucose transporter 2 from the cytosol to the plasma membrane. Similar results were observed in the liver of HFD-fed mice treated with apigenin. Collectively, our findings revealed that apigenin ameliorates obesity-induced insulin resistance in the liver by targeting fetuin-A.

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Section: Discussionmentioning

confidence: 99%

Apigenin targets fetuin-A to ameliorate obesity-induced insulin resistance

Hsu,

Chen,

Wang

et al. 2024

Int. J. Biol. Sci.

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SPR Biosensor for Quantification of Fetuin-A as a Promising Multibiomarker

Riedelová-Reicheltová¹,

Májek²,

Pecankova³

et al. 2018

Physiol Res

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Early diagnosis of ongoing malignant disease is crucial to improve survival rate and life quality of the patients and requires sensitive detection of specific biomarkers e.g. prostate-specific antigen (PSA), carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP), etc. In spite of current technological advances, malignant diseases are still identified in rather late stages, which have detrimental effect on the prognosis and treatment of the disease. Here, we present a biosensor able to detect fetuin-A, a potential multibiomarker. The biosensing platform is based on polymer brush combining antifouling monomer units of N-(2-hydroxypropyl)methacrylamide (HPMA) and carboxybetaine methacrylamide (CBMAA), statistically copolymerized by surface-initiated atom transfer radical polymerization. The copolymer poly(HPMA-co-CBMAA) exhibits excellent non-fouling properties in the most relevant biological media (i.e. blood plasma) as well as antithrombogenic surface properties by preventing the adhesion of blood components (i.e. leukocytes; platelets; and erythrocytes). Moreover, the polymer brush can be easily functionalized with biorecognition elements maintaining high resistance to blood fouling and the binding capacity can be regulated by tuning the ratio between CBMAA and HPMA units. The superior antifouling properties of the copolymer even after biofunctionalization were exploited to fabricate a new plasmonic biosensor for the analysis of fetuin-A in real clinical blood plasma samples. The assay used in this work can be explored as label-free affinity biosensor for diagnostics of different biomarkers in real clinical plasma samples and to shift the early biomarker detection toward novel biosensor technologies allowing point of care analysis.

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Corrigendum to “Facilitatory effects of fetuin-A on atherosclerosis” [Atherosclerosis 246 (2016) 344–351]

Cited by 2 publications

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Apigenin targets fetuin-A to ameliorate obesity-induced insulin resistance

Apigenin targets fetuin-A to ameliorate obesity-induced insulin resistance

SPR Biosensor for Quantification of Fetuin-A as a Promising Multibiomarker

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