The role of fetuin-A in cardiovascular diseases

Vörös, Krisztián; Cseh, Károly; Kopper, László

doi:10.1556/oh.2014.29793

Cited by 9 publications

(9 citation statements)

References 50 publications

(83 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies report that VC, arterial stiffness, and increased risk of mortality and CV events, are related to low serum levels of Fet-A [249][250][251][252][253], which is also decreased in dialysis patients and negatively correlates with valvular calcification and abdominal aortic calcification [254,255]. Low protein diets, which are low in phosphate, promote VC by lowering Fet-A while increasingly precipitating calcium-phosphate complexes, in the serum of an experimental uremic rat model [256].…”

Section: Fetuin-a (Fet-a)mentioning

confidence: 99%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

281

254

View full text Add to dashboard Cite

Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

show abstract

Section: Fetuin-a (Fet-a)mentioning

confidence: 99%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

281

254

View full text Add to dashboard Cite

show abstract

“…It serves as a natural inhibitor of tissue and vascular calcification and also as a protective factor in Atheriosclerosis [24]. The first documented observational studies on Fetuin-A is the one conducted on patients with enhanced kidney disease.…”

Section: Role Of Fetuin-a In Cardiovascular Diseasementioning

confidence: 99%

Fetuin-A: A Biomarker for Type II Diabetes Mellitus

Udeh¹

2017

IJBMR

View full text Add to dashboard Cite

Abstract:Fetuins are blood glycoproteins manufactured in the liver and secreted into the bloodstream. These glycoproteins make up a large group of binding proteins which mediates the transit and presence of a myriad of substances in the blood stream. Serum albumin, which is the most abundant protein in adult animal plasma is best known as the representative of these carrier proteins. In bone homeostasis, it is the circulating glycoprotein that plays a critical role. It plays major roles also in prevention of vascular calcification, disruption of adipocyte function and impairment of insulin signaling. Even with its major role, it is highly dependable in preventing and/or amplifying of the above disease processes. Certain diseases have been associated with high levels of Fetuin A. Although low levels of it in the plasma assist potentially in the protective effect of artery calcification in non-Chronic Kidney Disease (CKD) patients, high levels of the glycoprotein are the greatest concern in patients at higher risk of cardiovascular disease (CVD) and diabetes. The range of serum fetuin A in healthy adults is between 0.4 and 1mg/ml serum. The most studied function of fetuin A is mediated by the D1 domain. But the domain that binds with insulin receptor is yet to be known. The B chain consists of 27 amino acid residues which are distributed unevenly among the charged and neutral portion. Fetuins are proteins highly expressed in the liver blood plasma. They bear post translational modifications in proteolytic processing, phosphorylation, complex glycosylation and sulfation. The precussors of Fetuin A in humans are single-chained to the mature circulating double-chain form. In septicaemia and bovine, human fetuin A is perceptible to further proteolytic cleavage. Since the discovery of Fetuin A as a glycoprotein that inhibits vascular calcification in early 1990s, the biologic attributed roles has increased and still increasing exponentially. Apart from the roles it plays in type II diabetes mellitus and cardiovascular disease, other roles have been noted. Other effects and roles of Fetuin A are still being researched on.

show abstract

“…Bovine serum has been found to contain more fetuin than albumin, while adult serum contains more albumin than fetuin. This protein was described in humans in 1960 and known as "α2Heremans-Schmid glycoprotein" (AHSG) (1)(2)(3). This name is due to the fraction of alpha 2 globulin of serum proteins in cellulose acetate electrophoresis.…”

Section: Introductionmentioning

confidence: 99%

“…In fact, fetuin is a part of a large group of binding proteins mediating the transport and availability of a wide variety of cargo substances in the bloodstream (2). Fetuin-A is a glycoprotein, weighting of 64 kDA that is synthesized in the liver by hepatocytes (1). Fetuin-A gene exists on chromosomes 3q27 in the human.…”

Section: Introductionmentioning

confidence: 99%