2017
DOI: 10.4103/ijcep.ijcep_3_17
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Molecular mediators and controlling mechanism of vascular calcification

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Cited by 7 publications
(4 citation statements)
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“…The classically held view that mineralization is a passive, degenerative process must be dispelled nowadays as it turns out to be actively regulated akin to bone mineralization. 59,60 Regardless of the primarily altered blood electrolyte(s) in rats (Ca, IP, or both), the resulting histomorphological picture remains the same and is in accordance with the pattern described above.…”
Section: Monovalent Fgfr1-antagonist Induced Metastatic Mineralizatio...supporting
confidence: 74%
See 1 more Smart Citation
“…The classically held view that mineralization is a passive, degenerative process must be dispelled nowadays as it turns out to be actively regulated akin to bone mineralization. 59,60 Regardless of the primarily altered blood electrolyte(s) in rats (Ca, IP, or both), the resulting histomorphological picture remains the same and is in accordance with the pattern described above.…”
Section: Monovalent Fgfr1-antagonist Induced Metastatic Mineralizatio...supporting
confidence: 74%
“…The classically held view that mineralization is a passive, degenerative process must be dispelled nowadays as it turns out to be actively regulated akin to bone mineralization. 59,60…”
Section: Monovalent Fgfr1-antagonist Induced Metastatic Mineralizatio...mentioning
confidence: 99%
“…• увеличении продукции эндотелиального оксида азота (NO), • уменьшении адгезии и агрегации тромбоцитов, • снижении окислительного стресса, • регуляции мышечного тонуса сосудов, • уменьшении выделения вазоконстриктивных метаболитов, • подавлении высвобождения провоспалительных цитокинов, • модулировании иммунного ответа, • ингибировании пролиферации и миграции гладкомышечных клеток. В экспериментальных исследованиях доказано, что активный метаболит витамина D -1,25(ОН)2D уменьшает отложение минеральных депозитов во внутренней оболочке артерий, регулирует содержание в сыворотке крови кальция и фосфора [9][10][11]. Увеличение жесткости сосудистой стенки является важным фактором в развитии атеросклероза.…”
Section: âèòàìèí D è ðàçâèòèå àòåðîñêëåðîçàunclassified
“… 26 Given to its interaction with and neutralizing apoptotic factor TRAIL, it is considered as an anti-apoptotic factor, therefore, OPG acts as anti-calcifying agent in this background. 26 , 27 Studies show that OPG is the key regulator of bone remodeling by inhibition of interaction between RANKL, a specific receptor of RANK on cell surface. While the underlying molecular basis of signaling pathways in VC are not fully understood it has been shown that OPG deficient (OPG−/−) mouse models display calcification in renal arteries and aorta and also a reduction in bone mass accompanied by early onset osteoporosis.…”
Section: Introductionmentioning
confidence: 99%