Antioxidants and coronary artery disease

Faggiotto, Agostino; Poli, Andrea; Catapano, Alberico L.

doi:10.1097/00041433-199812000-00005

Cited by 25 publications

(15 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…So far, only a few small, prospective, epidemiological studies that evaluate the association between surrogate markers of oxidative stress and CVD are available in CKD patients (43,(125)(126)(127). This is in contrast to the larger number of prospective epidemiologic studies in the general population, which links low intake of dietary antioxidants to cardiovascular risk (128).…”

Section: Oxidative Stress-an Intricate But Promising Area In Ckdmentioning

confidence: 99%

Emerging Biomarkers for Evaluating Cardiovascular Risk in the Chronic Kidney Disease Patient

Stenvinkel¹,

Carrero²,

Axelsson³

et al. 2008

Clinical Journal of the American Society of Nephrology

491

373

View full text Add to dashboard Cite

Premature cardiovascular disease (CVD), including stroke, peripheral vascular disease, sudden death, coronary artery disease, and congestive heart failure, is a notorious problem in patients with chronic kidney disease (CKD). Because the presence of CVD is independently associated with kidney function decline, it appears that the relationship between CKD and CVD is reciprocal or bidirectional, and that it is this association that leads to the vicious circle contributing to premature death. As randomized, placebo-controlled trials have so far been disappointing and unable to show a survival benefit of various treatment strategies, such a lipid-lowering, increased dialysis dose and normalization of hemoglobin, the risk factor profile seems to be different in CKD compared with the general population. Indeed, seemingly paradoxical associations between traditional risk factors and cardiovascular outcome in patients with advanced CKD have complicated our efforts to identify the real cardiovascular culprits. This review focuses on the many new pieces that need to be fit into the complicated puzzle of uremic vascular disease, including persistent inflammation, endothelial dysfunction, oxidative stress, and vascular ossification. Each of these is not only highly prevalent in CKD but also more strongly linked to CVD in these patients than in the general population. However, a causal relationship between these new markers and CVD in CKD patients remains to be established. Finally, two novel disciplines, proteomics and epigenetics, will be discussed, because these tools may be helpful in the understanding of the discussed vascular risk factors.

show abstract

Section: Oxidative Stress-an Intricate But Promising Area In Ckdmentioning

confidence: 99%

Emerging Biomarkers for Evaluating Cardiovascular Risk in the Chronic Kidney Disease Patient

Stenvinkel¹,

Carrero²,

Axelsson³

et al. 2008

Clinical Journal of the American Society of Nephrology

491

373

View full text Add to dashboard Cite

show abstract

“…Antioxidants have been shown to slow down the atherosclerotic process, but their mechanisms of action are only poorly understood (Olsson & Yuan, 1996;Diaz, et al, 1997;Faggiotto et al, 1998). Antioxidants are able to modulate LDL oxidation (Heinecke, 1998), and also act at the cellular level by modulating the activity of various intracellular signalling pathways and inhibiting the pathogenic e ects (e.g.…”

Section: Introductionmentioning

confidence: 99%

Phenolic antioxidants trolox and caffeic acid modulate the oxidized LDL‐induced EGF‐receptor activation

Vacaresse

Vieira

Robbesyn

et al. 2001

British J Pharmacology

View full text Add to dashboard Cite

1 Oxidized low density lipoproteins (oxLDL) are thought to play a major role in atherosclerosis. OxLDL act in part through alteration of intracellular signalling pathways in cells of the vascular wall. We recently reported that the EGF receptor (EGFR) signalling pathway is activated by lipid peroxidation products (among them 4-hydroxynonenal, 4-HNE) contained in oxLDL. 2 The use of phenolic antioxidants, such as trolox, alpha-tocopherol, ca eic acid and tyrphostins A-25, A-46 or A-1478, showed that the oxLDL-induced EGFR activation is constituted by two separate components, the ®rst (early) one being antioxidant-insensitive, the second (late) being antioxidant-sensitive. 3 4-HNE derivatization of EGFR and EGFR activation induced by exogenous 4-HNE, suggest that the early (0.5 ± 3 h) component of oxLDL-induced EGFR activation is mediated (at least in part) by 4-HNE (and possibly by other oxidized lipids). This early component is antioxidantinsensitive. 4 The second component (4 ± 5 h) of the oxLDL-induced EGFR activation is antioxidant-sensitive, since it is blocked by antioxidants such as trolox, ca eic acid or PDTC, which act by blocking the cellular oxidative stress (H 2 O 2 generation) evoked by oxLDL. Conversely, exogenous H 2 O 2 induced EGFR autophosphorylation (thus mimicking the second component) and was also inhibited by antioxidants. This e ect is mediated in part through inhibition by oxidative stress of protein tyrosine phosphatases involved in EGFR dephosphorylation.

show abstract

“…In fact, various observational studies have suggested that the intake of antioxidant vitamins (vitamins C, E, etc.) is effective for the prevention of atherosclerotic diseases 28) . However, as many of the large-scale clinical studies performed recently presented negative views on a significant preventive effect of high-dose administration of vitamins C and E on atherosclerotic diseases, there are no solid grounds for recommending the intake of antioxidant vitamins in addition to regular meals for the prevention of the progression of atherosclerosis [29][30][31] .…”

Section: Smoking Cessationmentioning

confidence: 99%