This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Napoli, C. Articles by Sica, V. Search for Related Content PubMed PubMed Citation Articles by Napoli, C. Articles by Sica, V. Related Collections Other Vascular biology Related Article

(Circulation. 2005;111:1568-1570.)
© 2005 American Heart Association, Inc.

Editorial

Childhood Infection and Endothelial Dysfunction

A Potential Link in Atherosclerosis?

C. Napoli, MD, PhD, MBE; O. Pignalosa, MD; F. de Nigris, BiolD, PhD; V. Sica, MD

From the Department of General and Clinical Pathology (C.N., O.P., F.d.N., V.S.), Excellence Research Center on Cardiovascular Disease, II University of Naples, Naples, Italy; the Department of Pharmacology (F.d.N.), University of Salerno, Salerno, Italy; and the Whitaker Cardiovascular Institute and Evans Department of Medicine (C.N.), Boston University, Boston, Mass.

Correspondence to Claudio Napoli, MD, PhD, MBE, Department of General and Clinical Pathology II, Excellence Research Center on Cardiovascular Disease, II University of Naples, Naples, Italy. E-mail claunap@tin.it or claunap@bu.edu

Key Words: Editorials • pediatrics • atherosclerosis • infection

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The prodromal stage of atherosclerotic lesions (known as lipidotic fatty streak accumulation) is already formed during human fetal development.¹ Fatty streaks containing characteristic accumulations of lipids, lipid peroxidation products, and macrophages occur in the aorta of premature fetuses. Intimal thickening is also observed in fetal coronary arteries.^2,3 During infancy, fatty streaks become increasingly prevalent, and some of them progress to advanced stages of atherosclerotic lesions.^4–7 Once initiated, the progression of atherosclerosis is influenced by classic risk factors that promote vascular inflammation and plaque rupture. The observation that maternal hypercholesterolemia is associated with greatly enhanced fatty streak formation in fetal arteries¹ indicates that hypercholesterolemia may play a pathogenic role in early fetal atherosclerotic lesions. Maternal hypercholesterolemia is also able to influence fetal sterol metabolism during pregnancy in animal models.^8,9 Consistently, direct evidence for a causal role of maternal hypercholesterolemia and the involvement of oxidative stress has been obtained in a rabbit model^10,11 and in LDL receptor–deficient mice.¹² From a molecular standpoint, many signaling pathways are affected by increased oxidation of LDL or the intracellular formation of reactive oxygen species, and this phenomenon can be exacerbated by concomitant hypercholesterolemia.¹³ Interestingly, deletion of the p66shc longevity gene reduces systemic and tissue oxidative stress, vascular cell apoptosis, and early atherogenesis in mice fed a very highly hypercholesterolemic diet.¹⁴ Finally, growing evidence in the literature suggests that vascular damage occurs early and is mediated by polyunsaturated fatty acids secondary to a maternal hypercholesterolemic diet.^10,15–17 Nevertheless, it is not clear to what extent proteic undernutrition . . . [Full Text of this Article]

Related Article:

Endothelial Dysfunction in Childhood Infection

Marietta Charakida, Ann E. Donald, Mari Terese, Sam Leary, Julian P. Halcox, Andy Ness, George Davey Smith, Jean Golding, Peter Friberg, Nigel J. Klein, John E. Deanfield for the ALSPAC (Avon Longitudinal Study of Parents and Children) Study Team
Circulation 2005 111: 1660-1665. [Abstract] [Full Text]

This article has been cited by other articles:

				E. M. Urbina, R. V. Williams, B. S. Alpert, R. T. Collins, S. R. Daniels, L. Hayman, M. Jacobson, L. Mahoney, M. Mietus-Snyder, A. Rocchini, et al. Noninvasive Assessment of Subclinical Atherosclerosis in Children and Adolescents: Recommendations for Standard Assessment for Clinical Research: A Scientific Statement From the American Heart Association Hypertension, November 1, 2009; 54(5): 919 - 950. [Abstract] [Full Text] [PDF]

				A. Kontush and M. J. Chapman Functionally Defective High-Density Lipoprotein: A New Therapeutic Target at the Crossroads of Dyslipidemia, Inflammation, and Atherosclerosis Pharmacol. Rev., September 1, 2006; 58(3): 342 - 374. [Abstract] [Full Text] [PDF]