Effects of fetuin-A with diverse functions and multiple mechanisms on human health

İçer, Mehmet Arif; Yıldıran, Hilal

doi:10.1016/j.clinbiochem.2020.11.004

Cited by 32 publications

(31 citation statements)

References 132 publications

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“…Fetuin-A is a hepatic secretory glycoprotein that on the one hand promotes insulin resistance by inhibiting the insulin receptor tyrosine kinase in skeletal muscle and hepatocytes, serving as an adaptor protein for saturated fatty acids and allowing them to activate Toll-like receptor 4 (TLR4), thereby inducing inflammatory signaling and insulin resistance [ 1 , 2 ]. Another possible link between fetuin-A and insulin resistance is fetuin-A-stimulated inflammation in pancreatic adipocytes and islets, and fetuin-A-mediated c-Jun N-terminal kinase- and Ca-dependent impairment of insulin secretion [ 3 , 4 ]. On the other hand, fetuin-A inhibits soft tissue calcification [ 5 – 7 ] through binding of small clusters of calcium and phosphate, preventing their growth, aggregation and mineral precipitation, stabilizing these ions and preventing their uptake by cells [ 4 , 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

“…Another possible link between fetuin-A and insulin resistance is fetuin-A-stimulated inflammation in pancreatic adipocytes and islets, and fetuin-A-mediated c-Jun N-terminal kinase- and Ca-dependent impairment of insulin secretion [ 3 , 4 ]. On the other hand, fetuin-A inhibits soft tissue calcification [ 5 – 7 ] through binding of small clusters of calcium and phosphate, preventing their growth, aggregation and mineral precipitation, stabilizing these ions and preventing their uptake by cells [ 4 , 7 , 8 ]. These soluble protein-mineral colloids known as calciprotein particles are subsequently cleared by the reticuloendothelial system.…”

Section: Introductionmentioning

confidence: 99%

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Fetuin-A and risk of diabetes-related vascular complications: a prospective study

Birukov

Polemiti

Jäger

et al. 2022

Cardiovasc Diabetol

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Background Fetuin-A is a hepatokine which has the capacity to prevent vascular calcification. Moreover, it is linked to the induction of metabolic dysfunction, insulin resistance and associated with increased risk of diabetes. It has not been clarified whether fetuin-A associates with risk of vascular, specifically microvascular, complications in patients with diabetes. We aimed to investigate whether pre-diagnostic plasma fetuin-A is associated with risk of complications once diabetes develops. Methods Participants with incident type 2 diabetes and free of micro- and macrovascular disease from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam cohort (n = 587) were followed for microvascular and macrovascular complications (n = 203 and n = 60, respectively, median follow-up: 13 years). Plasma fetuin-A was measured approximately 4 years prior to diabetes diagnosis. Prospective associations between baseline fetuin-A and risk of complications were assessed with Cox regression. Results In multivariable models, fetuin-A was linearly inversely associated with incident total and microvascular complications, hazard ratio (HR, 95% CI) per standard deviation (SD) increase: 0.86 (0.74; 0.99) for total, 0.84 (0.71; 0.98) for microvascular and 0.92 (0.68; 1.24) for macrovascular complications. After additional adjustment for cardiometabolic plasma biomarkers, including triglycerides and high-density lipoprotein, the associations were slightly attenuated: 0.88 (0.75; 1.02) for total, 0.85 (0.72; 1.01) for microvascular and 0.95 (0.67; 1.34) for macrovascular complications. No interaction by sex could be observed (p > 0.10 for all endpoints). Conclusions Our data show that lower plasma fetuin-A levels measured prior to the diagnosis of diabetes may be etiologically implicated in the development of diabetes-associated microvascular disease.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fetuin-A and risk of diabetes-related vascular complications: a prospective study

Birukov

Polemiti

Jäger

et al. 2022

Cardiovasc Diabetol

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“…In serum, fetuin A forms soluble, unstable complexes with calcium ions and phosphate ions. By forming these complexes, it seems that fetuin A could be involved in initiating calcium deposits (calcification) found in coronary heart disease, while having an opposite effect in peripheral arterial pathologies, namely, protection against atherosclerosis [ 64 ]. The higher risk of developing cardiovascular pathologies in the elderly with high serum levels of Fetuin-A is in fact associated with a much higher risk of developing obesity, T2DM and dyslipidemias (because fetuin A has the ability to reduce lipogenesis and to accentuate the lipolysis process) [ 65 ].…”

Section: Diabetes Mellitus and Cardiovascular Disease In Elderly Patientsmentioning

confidence: 99%

Cardiovascular Risk Factors and Physical Activity for the Prevention of Cardiovascular Diseases in the Elderly

Milaciu

Negrean

Orășan

et al. 2021

IJERPH

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Cardiovascular diseases create an important burden on the public health systems, especially in the elderly, mostly because this group of patients frequently suffer from multiple comorbidities. Accumulating cardiovascular risk factors during their lifetime has a detrimental effect on an older adult‘s health status. The modifiable and non-modifiable cardiovascular risk factors are very diverse, and are frequently in a close relationship with the metabolic comorbidities of the elderly, mainly obesity and Diabetes Mellitus. In this review, we aim to present the most important cardiovascular risk factors which link aging and cardiovascular diseases, starting from the pathophysiological links between these factors and the aging process. Next, we will further review the main interconnections between obesity and Diabetes Mellitus and cardiovascular diseases of the elderly. Lastly, we consider the most important aspects related to prevention through lifestyle changes and physical activity on the occurrence of cardiovascular diseases in the elderly.

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“…The secreted content of MGP in these calcified exosomes secreted during VC is low, whereas the hydroxyapatite content is high, which is also the initiating factor that leads to mineral deposition in the formation of microcalcification (26). The low concentrations of fetuin-A and Gla rich protein (GRP) in calcified exosomes causes them to aggregate in the collagen-sparse region to form microcalcifications upon release into the ECM (52). In addition to minerals in exosomes, external PS can also bind to calcium ion binding proteins, such as annexin A2, A5, and A6, thus forming hydroxyapatite deposition in the inner or outer part of the exosome membrane; thus, the exosomes transform into primary foci for calcification by providing mineral nucleation sites (48,53).…”

Section: Exosomes Promote Extracellular Mineral Deposits To Induce Vcmentioning

confidence: 99%

A narrative review of exosomes in vascular calcification

Zheng¹,

Liao²,

Xiong³

et al. 2021

Ann Transl Med

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Vascular calcification (VC) is the abnormal deposition of calcium, phosphorus, and other minerals in the vessel wall and can be commonly observed in diabetes, chronic kidney disease, and chronic inflammatory disease. It is closely associated with mortality from cardiovascular events. Traditionally, calcification is considered as a degenerative disease associated with the aging process, while increasing evidence has shown that the occurrence and development of calcification is an active biological process, which is highly regulated by multiple factors. The molecular mechanisms of VC have not yet been fully elucidated. Exosomes, as important transporters of substance transport and intercellular communication, have been shown to participate in VC. The regulation of VC by exosomes involves a number of complex biological processes, which occur through a variety of interaction mechanisms. However, the specific role and mechanism of exosomes in the process of VC are still not fully understood and require further study. This review will briefly describe the roles of exosomes in the process of VC including in the promotion of extracellular mineral deposits, induction of phenotypic conversion of vascular smooth muscle cells (VSMCs), transport of microRNA between cells, and regulation on autophagy and oxidative stress, with the aim of providing novel ideas for the clinical diagnosis and treatment of VC.

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Effects of fetuin-A with diverse functions and multiple mechanisms on human health

Cited by 32 publications

References 132 publications

Fetuin-A and risk of diabetes-related vascular complications: a prospective study

Fetuin-A and risk of diabetes-related vascular complications: a prospective study

Cardiovascular Risk Factors and Physical Activity for the Prevention of Cardiovascular Diseases in the Elderly

A narrative review of exosomes in vascular calcification

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