Vascular calcification; Stony bridge between kidney and heart

Zaker, Behzad; Ardalan, Mohammadreza

doi:10.34172/jcvtr.2020.29

Cited by 4 publications

(3 citation statements)

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“…[23][24][25] Characterized by reduced arterial wall elasticity and blocked blood flow, it can lead to heart attack and stroke. [26][27][28] VC is thought to be a regulatory process, similar in many ways to bone mineralization. 29 Vascular cells such as VSMCs and pericyclic-like cells play an important role in VC .…”

Section: Discussionmentioning

confidence: 99%

Ligustrazine activate the PPAR-γ pathway and play a protective role in vascular calcification

Li¹,

Yang

2021

Vascular

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Objective The purpose of this study was to explore the role of ligustrazine in vascular calcification. Methods After β-GP stimulation, vascular smooth muscle cells (VSMCs) were detected by Alizarin Red Staing staining. Calcium content and alkaline phosphatase (ALP) activity were detected by intracellular calcium assay kit and ALP assay kit, respectively. The expression of peroxisome proliferation-activated receptor (PPAR-γ) pathway–related proteins was detected by Western blot. PPAR-γ, MSX2, osteopontin (OPN), sclerostin, and BGP were detected by RT-PCR. Results β-GP induced the decreased activity and expression of PPAR-γ and ALP in VSMCs, while ligustrazine activated the expression of PPAR-γ. Through activation of PPAR-γ, ligustrazine decreased β-GP–induced VSMC calcification, decreased the expression of markers of osteogenesis and chondrogenic differentiation, and increased the expression of VSMC markers. Conclusion Ligustrazine activates the PPAR-γ pathway and plays a protective role in vascular calcification.

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Section: Discussionmentioning

confidence: 99%

Ligustrazine activate the PPAR-γ pathway and play a protective role in vascular calcification

Li¹,

Yang

2021

Vascular

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“…Importantly, in addition to a genetic background, the altered balance between calcification contributors ( 73 – 80 ) ( Figure 2 ) and circulating or tissue calcification inhibitors ( 81 – 88 ) ( Figure 2 ) makes CKD patients more or less susceptible to accelerated VC. Different comorbid pathologies associated with intimal atheroma calcification (ischemic events), arteriosclerosis (arterial stiffening), and heart valvular calcification may be overlapping, and CKD predisposes to all these types of VC ( 54 , 64 ). Finally, the revolution in omics technology (genomics, epigenomics, transcriptomics, proteomics, and metabolomics) has resulted in the accumulation of cellular and molecular-level data ( 63 , 67 ) which will provide novel approaches on the mechanisms associated with VC ( 63 , 67 ).…”

Section: Pathophysiology Of Ckd-mbd-related Vascular Calcificationmentioning

confidence: 99%

Clinical Approach to Vascular Calcification in Patients With Non-dialysis Dependent Chronic Kidney Disease: Mineral-Bone Disorder-Related Aspects

et al. 2021

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Chronic kidney disease (CKD) is associated with a very high morbimortality, mainly from cardiovascular origin, and CKD is currently considered in the high- or very high risk- cardiovascular risk category. CKD-mineral and bone disorders (CKD-MBDs), including vascular and/or valvular calcifications, are also associated with these poor outcomes. Vascular calcification (VC) is very prevalent (both intimal and medial), even in non-dialysis dependent patients, with a greater severity and more rapid progression. Simple X-ray based-scores such as Adragão's (AS) are useful prognostic tools and AS (even AS based on hand-X-ray only) may be superior to the classic Kauppila's score when evaluating non-dialysis CKD patients. Thus, in this mini-review, we briefly review CKD-MBD-related aspects of VC and its complex pathophysiology including the vast array of contributors and inhibitors. Furthermore, although VC is a surrogate marker and is not yet considered a treatment target, we consider that the presence of VC may be relevant in guiding therapeutic interventions, unless all patients are treated with the mindset of reducing the incidence or progression of VC with the currently available armamentarium. Avoiding phosphate loading, restricting calcium-based phosphate binders and high doses of vitamin D, and avoiding normalizing (within the normal limits for the assay) parathyroid hormone levels seem logical approaches. The availability of new drugs and future studies, including patients in early stages of CKD, may lead to significant improvements not only in patient risk stratification but also in attenuating the accelerated progression of VC in CKD.

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“…Наследственная предрасположенность также вносит весомый вклад в развитие сосудистой кальцификации, анализ сцепления показал связь с ней множественных локусов и генов [5].…”

Section: Introductionunclassified

Biomarkers of vascular calcification: their relationship with diseases of the cardiovascular system and their importance in clinical practice

Маслацов

Ragino

2021

jour

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Данный литературный обзор посвящен актуальным проблемам сосудистой кальцификации с акцентом на связи некоторых биохимических маркеров сосудистой кальцификации (в приоритете остеопротегерин и остеопонтин) с сердечно-сосудистыми заболеваниями и другими ассоциированными состояниями. Также многие аспекты нижеприведенных исследований имеют непосредственно прикладной, клинический характер, а некоторые положения помогают внести ясность в патофизиологию сосудистой кальцификации. Цель настоящего обзора -обобщение и систематизация актуальных знаний о вкладе биохимических маркеров сосудистой кальцификации в патологические процессы, происходящие в сосудистой стенке и приводящие в конечном итоге сосудистого континуума к сердечно-сосудистым событиям. В обзоре представлены самые современные данные отечественных и зарубежных исследований, посвящённые сосудистой кальцификации. Для его подготовки использованы базы данных PubMed, Google Scholar, ScienceDirect, MDPI, Hindawi, Oxford Academic.

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Vascular calcification; Stony bridge between kidney and heart

Cited by 4 publications

References 61 publications

Ligustrazine activate the PPAR-γ pathway and play a protective role in vascular calcification

Ligustrazine activate the PPAR-γ pathway and play a protective role in vascular calcification

Clinical Approach to Vascular Calcification in Patients With Non-dialysis Dependent Chronic Kidney Disease: Mineral-Bone Disorder-Related Aspects

Biomarkers of vascular calcification: their relationship with diseases of the cardiovascular system and their importance in clinical practice

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