Mechanisms of Arterial Calcification: The Role of Matrix Vesicles

Zazzeroni, Luca; Faggioli, Gianluca; Pasquinelli, Gianandrea

doi:10.1016/j.ejvs.2017.12.009

Cited by 80 publications

(60 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In VC, Fet-A is an inhibitor of calcification, which acts by protecting cells from crystal growth or deposition [257]. In this context, Fet-A is considered an important regulator of both bone resorption and VC.…”

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

“…In fact, apoptosis occurs in VSMCs before the onset of calcification and VSMC "blebs" or apoptotic bodies probably concentrate calcium in a crystallized form [41]. Increasing evidence also show that VSMCs undergoing osteogenic transformation promote calcification by releasing matrix vesicles capable of nucleating hydroxyapatite [42]. Zhang et al [43] demonstrated that Sp1 gene silencing delayed vascular calcification by inhibiting the processes of phenotype switch, apoptosis and matrix vesicle release in VMSCs.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Gastrin-Releasing Peptide Attenuates Phosphate-Induced Vascular Calcification

Park

Kim

Hwang

et al. 2020

Cells

View full text Add to dashboard Cite

Vascular calcification is the pathological deposition of calcium/phosphate in the vascular system and is closely associated with cardiovascular morbidity and mortality. Here, we investigated the role of gastrin-releasing peptide (GRP) in phosphate-induced vascular calcification and its potential regulatory mechanism. We found that the silencing of GRP gene and treatment with the GRP receptor antagonist, RC-3095, attenuated the inorganic phosphate-induced calcification of vascular smooth muscle cells (VSMCs). This attenuation was caused by inhibiting phenotype change, apoptosis and matrix vesicle release in VSMCs. Moreover, the treatment with RC-3095 effectively ameliorated phosphate-induced calcium deposition in rat aortas ex vivo and aortas of chronic kidney disease in mice in vivo. Therefore, the regulation of the GRP-GRP receptor axis may be a potential strategy for treatment of diseases associated with excessive vascular calcification.

show abstract

“…Molecular vascular calcification mechanisms are a complex intersection of regulatory pathways, including adenosine signaling, osteochondrogenesis, inflammation, endocrine pathways, hypoxia, malnutrition, autophagy, phosphate transport, and phosphate signaling. Please see these recent reviews for current detail on cardiovascular calcification mechanisms (Wu et al, 2013 ; Hortells et al, 2018 ; Zazzeroni et al, 2018 ).…”

Section: Calcific Potential Of the Placentamentioning

confidence: 99%

Placental Vascular Calcification and Cardiovascular Health: It Is Time to Determine How Much of Maternal and Offspring Health Is Written in Stone

et al. 2018

View full text Add to dashboard Cite

Vascular calcification is the deposition of calcium phosphate minerals in vascular tissue. Vascular calcification occurs by both active and passive processes. Extent and tissue-specific patterns of vascular calcification are predictors of cardiovascular morbidity and mortality. The placenta is a highly vascularized organ with specialized vasculature that mediates communication between two circulatory systems. At delivery the placenta often contains calcified tissue and calcification can be considered a marker of viral infection, but the mechanisms, histoanatomical specificity, and pathophysiological significance of placental calcification are poorly understood. In this review, we outline the current understanding of vascular calcification mechanisms, biomedical consequences, and therapeutic interventions in the context of histoanatomical types. We summarize available placental calcification data and clinical grading systems for placental calcification. We report on studies that have examined the association between placental calcification and acute adverse maternal and fetal outcomes. We then review the intersection between placental dysfunction and long-term cardiovascular health, including subsequent occurrence of maternal vascular calcification. Possible maternal phenotypes and trigger mechanisms that may predispose for calcification and cardiovascular disease are discussed. We go on to highlight the potential diagnostic value of placental calcification. Finally, we suggest avenues of research to evaluate placental calcification as a research model for investigating the relationship between placental dysfunction and cardiovascular health, as well as a biomarker for placental dysfunction, adverse clinical outcomes, and increased risk of subsequent maternal and offspring cardiovascular events.

show abstract

Mechanisms of Arterial Calcification: The Role of Matrix Vesicles

Cited by 80 publications

References 38 publications

Vascular Calcification—New Insights into Its Mechanism

Vascular Calcification—New Insights into Its Mechanism

Inhibition of Gastrin-Releasing Peptide Attenuates Phosphate-Induced Vascular Calcification

Placental Vascular Calcification and Cardiovascular Health: It Is Time to Determine How Much of Maternal and Offspring Health Is Written in Stone

Contact Info

Product

Resources

About