Inflammation and genetics are prominent mechanisms in the pathogenesis of atherosclerosis (AT) and its complications. In this review we discuss the possible impact on AT development of several genetic determinants involved in inflammation, oxidative stress and cytoprotection (IL-6, TNF-alpha, IL-10, CD14, TLR4, MT, HSP70). Genetic polymorphisms of these genes may affect a differential inflammatory response predisposing to AT. However, allelic polymorphisms of genes which increase the risk of AT frequently occur in the general population but, only adequate gene-environment-polymorphism interactions promote the onset of the disease. Zinc deficiency has been suggested as an environmental risk factor for AT. With advancing age, the incidence of zinc deficiency increases for several reasons. Among them, dietary intake, malabsorption and genetic background of inflammatory markers may be involved. A crucial contribution may also be played by increased oxidative stress which may lead to the appearance of dysfunctional proteins, including metallothioneins (MT) that are in turn involved in zinc homeostasis. The detection of candidate genes related to inflammation and promoting AT and their reciprocal influence/interaction with zinc status might allow earlier appropriate dietary interventions in genetically susceptible subjects.

GIACCONI, R., CARUSO, C., MALAVOLTA, M., LIO, D., BALISTRERI, C.R., SCOLA, L., et al. (2008). Pro-inflammatory genetic background and zinc status in old atherosclerotic subjects. AGEING RESEARCH REVIEWS, 7, 306-318 [10.1016/j.arr.2008.06.001].

Pro-inflammatory genetic background and zinc status in old atherosclerotic subjects.

GIACCONI, Robertina;CARUSO, Calogero;LIO, Domenico;BALISTRERI, Carmela Rita;SCOLA, Letizia;CANDORE, Giuseppina;
2008-01-01

Abstract

Inflammation and genetics are prominent mechanisms in the pathogenesis of atherosclerosis (AT) and its complications. In this review we discuss the possible impact on AT development of several genetic determinants involved in inflammation, oxidative stress and cytoprotection (IL-6, TNF-alpha, IL-10, CD14, TLR4, MT, HSP70). Genetic polymorphisms of these genes may affect a differential inflammatory response predisposing to AT. However, allelic polymorphisms of genes which increase the risk of AT frequently occur in the general population but, only adequate gene-environment-polymorphism interactions promote the onset of the disease. Zinc deficiency has been suggested as an environmental risk factor for AT. With advancing age, the incidence of zinc deficiency increases for several reasons. Among them, dietary intake, malabsorption and genetic background of inflammatory markers may be involved. A crucial contribution may also be played by increased oxidative stress which may lead to the appearance of dysfunctional proteins, including metallothioneins (MT) that are in turn involved in zinc homeostasis. The detection of candidate genes related to inflammation and promoting AT and their reciprocal influence/interaction with zinc status might allow earlier appropriate dietary interventions in genetically susceptible subjects.
2008
GIACCONI, R., CARUSO, C., MALAVOLTA, M., LIO, D., BALISTRERI, C.R., SCOLA, L., et al. (2008). Pro-inflammatory genetic background and zinc status in old atherosclerotic subjects. AGEING RESEARCH REVIEWS, 7, 306-318 [10.1016/j.arr.2008.06.001].
File in questo prodotto:
File Dimensione Formato  
AGEING.pdf

Solo gestori archvio

Descrizione: Articolo
Dimensione 429.5 kB
Formato Adobe PDF
429.5 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

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/10447/46625
Citazioni
  • ???jsp.display-item.citation.pmc??? 7
  • Scopus 26
  • ???jsp.display-item.citation.isi??? 19
social impact