Vascular Calcification in Uremia: New-Age Concepts about an Old-Age Problem

Smith, Edwin R.

doi:10.1007/978-1-4939-3353-2_13

Cited by 35 publications

(20 citation statements)

References 212 publications

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“…Therefore, a model of TM phenotype was successfully reproduced in this study. Our results also confirmed that human NPs were the known agents of emerging infectious diseases and producing apatite, which agrees well with other reports [ 14 , 15 ]. A possible calcification mechanism might be NP colonization in seminiferous tubules inducing an immune response, promoting inflammation development and further calcification.…”

Section: Discussionsupporting

confidence: 93%

Role of calcifying nanoparticles in the development of testicular microlithiasis in vivo

Lin

Gao

et al. 2017

BMC Urol

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BackgroundCalcifying nanoparticles (NPs) have been proven to be associated with a variety of pathological calcification and previously detected in semen samples from patients with testicular microlithiasis (TM). The present study was designed to test the hypothesis if human-derived NPs could invade the seminiferous tubules and induce TM phenotype.MethodsThe animals were divided into three groups. Normal saline (0.2 mL) was injected into the proximal right ductus deferens in group A as a control group. The experimental groups, B and C received Escherichia coli (106 cfu/mL, 0.2 mL) and human-derived NPs suspension (0.2 mL), respectively. Rats were euthanized in 2 batches at 2 and 4 weeks. Testicular pathology, ultrastructure and inflammatory mediators were assessed.ResultsChronic inflammatory changes were observed at 2 weeks in both groups B and C. Moreover, the innermost layer of sperm cells were structurally impaired and a zone of concentrically layered collagen fibers around the human NPs body was formed in the lumen of the seminiferous tubule in group C only, in which TM phenotype of remarkable calcification surrounded by cellular debris within the seminiferous tubules was built at 4 weeks.ConclusionsThe results obtained from our study suggested a potential pathogenic effect of NPs in the development of calcification within the seminiferous tubules, which should be addressed in the future studies.

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Section: Discussionsupporting

confidence: 93%

Role of calcifying nanoparticles in the development of testicular microlithiasis in vivo

Lin

Gao

et al. 2017

BMC Urol

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“…VC, abnormal deposition of calcium-phosphate (Pi) salts in vascular tissues including blood vessels, valves, and heart, is frequently observed in aging, diabetes mellitus, CKD, calcific aortic valve disease (CAVD), and several genetic diseases [5–8]. Mounting clinical evidence has shown that VC is indeed an independent predictor of cardiovascular morbidity and mortality in CKD and ESKD [9–11].…”

Section: Cardiovascular Mortality and Vascular Calcification (Vc)mentioning

confidence: 99%

Vascular calcification in CKD-MBD: Roles for phosphate, FGF23, and Klotho

Yamada

Giachelli

2017

Bone

255

196

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Vascular calcification (VC) is highly prevalent in aging, diabetes mellitus, and chronic kidney disease (CKD). VC is a strong predictor of cardiovascular morbidity and mortality in the CKD population. Complex pathological mechanisms are involved in the development of VC, including osteochondrogenic differentiation and apoptosis of vascular smooth muscle cells, instability and release of extracellular vesicles loaded calcium and phosphate, and elastin degradation. Elevated serum phosphate is a late manifestation of CKD, and has been shown to accelerate mineral deposition in both the vessel wall and heart valves. α-Klotho and fibroblast growth factor 23 (FGF23) are emerging factors in CKD-mineral and bone disorder (CKD-MBD) and are thought to be involved in the pathogenesis of uremic VC. There are discordant reports regarding the biomedical effects of FGF23 on VC. In contrast, mounting evidence supports a well-supported protective role for α-Klotho on VC. Further studies are warranted to elucidate potential roles of FGF23 and α-Klotho in VC and to determine where and how they are synthesized in normal and disease conditions. A thorough systemic evaluation of the biomedical interplay of phosphate, FGF23, and α-Klotho may potentially lead to new therapeutic options for patients with CKD-MBD.

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“…The formation of VC is associated with complex pathological mechanisms, including osteochondral differentiation and apoptosis of vascular smooth muscle cells (VSMCs), instability and release of extracellular vesicles loaded calcium and phosphate . Among the various causes in CKD, abnormal deposition of calcium phosphate (Pi) salt is most closely related to VC . It has been proved that elevated serum Pi is a risk factor for VC and cardiovascular mortality and morbidity among CKD populations in clinical studies .…”

Section: Introductionmentioning

confidence: 99%

“…1,7 Among the various causes in CKD, abnormal deposition of calcium phosphate (Pi) salt is most closely related to VC. 8 It has been proved that elevated serum Pi is a risk factor for VC and cardiovascular mortality and morbidity among CKD populations in clinical studies. 9,10 Therefore, it is of great significance to study the specific molecular mechanism of VSMCs calcification induced by high phosphorus in CKD.…”

Section: Introductionmentioning

confidence: 99%

Klotho/FGF23 axis mediates high phosphate‐induced vascular calcification in vascular smooth muscle cells via Wnt7b/β‐catenin pathway

Chen

Huang

Duan

et al. 2019

The Kaohsiung J of Med Scie

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Vascular calcification (VC) plays as a critical role on cardiovascular disease (CVD) and acts as a notable risk factor in cardiovascular system. Vascular smooth muscle cells (VSMCs) calcification can be triggered by high phosphate treatment; however, the explicit mechanism remains unclear. In the present study, we isolated VSMCs from primary rat artery, applied β‐GP (β‐glycerophosphate) for inducing VSMCs calcification in vitro to explore the mechanism of phosphate‐induced calcification in VSMCs. Alizarin red staining was performed to assess the mineralization in VSMCs. Calcium deposition experiment was taken to evaluate the calcium content. ALP staining was determined to assess the ALP activity. The recombinant adenoviruses were constructed for the overexpression of Klotho and FGF23, respectively. qRT‐PCR and western blot analysis were subjected to measure the expression of Klotho/FGF23 and correlated genes among Wnt7b/β‐catenin pathway. We found that the calcium content was obviously increased and Alizarin red staining was positive in calcification group exposure with high phosphate in a time‐dependent manner. The expression of Klotho and FGF23 was significantly decreased in the calcification group. However, overexpression of Klotho and FGF23 markedly reversed VSMCs calcification stimulating with high phosphate treatment. Moreover, Wnt7b/β‐catenin inhibitor DKK1 could partly attenuate the effect of high phosphate on calcified VSMCs. These findings demonstrated that Klotho/FGF23 axis could modulate high phosphate‐induced VSMCs calcification via Wnt7b/β‐catenin signaling pathway. Our findings unravel that Klotho/FGF23‐ Wnt7b/β‐catenin axis functions as a crucial role in the VSMCs calcification.

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Vascular Calcification in Uremia: New-Age Concepts about an Old-Age Problem

Cited by 35 publications

References 212 publications

Role of calcifying nanoparticles in the development of testicular microlithiasis in vivo

Role of calcifying nanoparticles in the development of testicular microlithiasis in vivo

Vascular calcification in CKD-MBD: Roles for phosphate, FGF23, and Klotho

Klotho/FGF23 axis mediates high phosphate‐induced vascular calcification in vascular smooth muscle cells via Wnt7b/β‐catenin pathway

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