Vitamin D represents a group of secosteroids involved in the calcium and phosphate metabolism. The active form of vitamin D, 1,25-dihydroxylcalciferol, exerts its biological mechanisms via the VDR (vitamin D receptor) which acts as a regulator of several target genes. Hypovitaminosis D is associated with many diseases, which are not only limited to the metabolism of the skeleton, but growing evidence links the deficit of vitamin D to cardiovascular, metabolic, immune, and neoplastic diseases. In regard to the cardiovascular system, current evidence shows the presence of VDR in endothelial cells. Moreover, both in vitro and animal experimental models demonstrated that the deficit of vitamin D can promote endothelial dysfunction and atherosclerosis development. Vitamin D can interfere with vascular functions also by affecting the production of vasodilator mediators. VDR is also expressed in left ventricle cardiomyocytes, and hypovitaminosis D can relate to cardiac hypertrophy and heart failure. Randomized clinical trials (RCT) designed to prove the therapeutic role of vitamin D supplementation have been inconclusive to date. The aim of this review is to highlight the main interactions between vitamin D metabolism and cardiovascular diseases; thus, focusing on pathogenic mechanisms and related clinical manifestations.

Role of vitamin D in cardiovascular diseases / Condoleo, Valentino; Pelaia, Corrado; Armentaro, Giuseppe; Severini, Giandomenico; Clausi, Elvira; Cassano, Velia; Miceli, Sofia; Vanessa Fiorentino, Teresa; Succurro, Elena; Arturi, Franco; Andreozzi, Francesco; Sesti, Giorgio; Sciacqua, Angela. - In: ENDOCRINES. - ISSN 2673-396X. - 2:(2021), pp. 417-426. [10.3390/endocrines2040037]

Role of vitamin D in cardiovascular diseases

Giorgio Sesti
Penultimo
Supervision
;
2021

Abstract

Vitamin D represents a group of secosteroids involved in the calcium and phosphate metabolism. The active form of vitamin D, 1,25-dihydroxylcalciferol, exerts its biological mechanisms via the VDR (vitamin D receptor) which acts as a regulator of several target genes. Hypovitaminosis D is associated with many diseases, which are not only limited to the metabolism of the skeleton, but growing evidence links the deficit of vitamin D to cardiovascular, metabolic, immune, and neoplastic diseases. In regard to the cardiovascular system, current evidence shows the presence of VDR in endothelial cells. Moreover, both in vitro and animal experimental models demonstrated that the deficit of vitamin D can promote endothelial dysfunction and atherosclerosis development. Vitamin D can interfere with vascular functions also by affecting the production of vasodilator mediators. VDR is also expressed in left ventricle cardiomyocytes, and hypovitaminosis D can relate to cardiac hypertrophy and heart failure. Randomized clinical trials (RCT) designed to prove the therapeutic role of vitamin D supplementation have been inconclusive to date. The aim of this review is to highlight the main interactions between vitamin D metabolism and cardiovascular diseases; thus, focusing on pathogenic mechanisms and related clinical manifestations.
2021
Vitamin D; cardiovascular disease; endothelial dysfunction; atherosclerosis; arterial hypertension; heart failure
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Role of vitamin D in cardiovascular diseases / Condoleo, Valentino; Pelaia, Corrado; Armentaro, Giuseppe; Severini, Giandomenico; Clausi, Elvira; Cassano, Velia; Miceli, Sofia; Vanessa Fiorentino, Teresa; Succurro, Elena; Arturi, Franco; Andreozzi, Francesco; Sesti, Giorgio; Sciacqua, Angela. - In: ENDOCRINES. - ISSN 2673-396X. - 2:(2021), pp. 417-426. [10.3390/endocrines2040037]
File allegati a questo prodotto
File Dimensione Formato  
Condoleo_Role-of-Vitamine_2021.pdf

accesso aperto

Tipologia: Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza: Creative commons
Dimensione 291.19 kB
Formato Adobe PDF
291.19 kB Adobe PDF

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1648071
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 101
  • ???jsp.display-item.citation.isi??? 97
social impact