Short telomeres protect from diet-induced atherosclerosis in apolipoprotein E-null mice.

Enric Poch, Paz Carbonell, Sonia Franco, Antonio Díez-Juan, María A. Blasco, Vicente Andrés

Research output: Contribution to journalArticle

Abstract

By imposing a replicative defect in most somatic cells, gradual telomere attrition during aging is thought to progressively impair cellular function and viability and may contribute to age-related disease. Immune cells play important roles in all phases of atherosclerosis, a multifactorial disease that prevails within the elderly. Because shorter telomeres have been found in circulating blood leukocytes of human patients with advanced coronary atherosclerosis, it has been suggested that telomere shortening may predispose the organism to atheroma development. In this study, we assessed the impact of telomere attrition on atherogenesis induced by dietary cholesterol in apolipoprotein E (apoE)-deficient mice, a well-established model of experimental atherosclerosis that recapitulates important aspects of the human disease. Our study shows that late-generation mice doubly deficient in apoE and telomerase RNA experience telomere attrition and a substantial reduction of atherosclerosis compared with control mice with intact telomerase, in spite of sustained hypercholesterolemia in response to the atherogenic diet. Short telomeres impaired the proliferation of both lymphocytes and macrophages, an important step in atherosclerosis development. Therefore, telomere exhaustion resulting in replicative immunosenescence may serve as a mechanism for restricting atheroma progression.

Original languageEnglish (US)
Pages (from-to)418-420
Number of pages3
JournalFASEB Journal
Volume18
Issue number2
StatePublished - 2004
Externally publishedYes

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Telomere
Apolipoproteins E
Nutrition
Atherosclerosis
Diet
Dietary Cholesterol
Lymphocytes
Macrophages
Telomerase
Atherosclerotic Plaques
Blood
Aging of materials
Atherogenic Diet
Telomere Shortening
Defects
Hypercholesterolemia
Coronary Artery Disease
Leukocytes
Theoretical Models

Cite this

Poch, E., Carbonell, P., Franco, S., Díez-Juan, A., Blasco, M. A., & Andrés, V. (2004). Short telomeres protect from diet-induced atherosclerosis in apolipoprotein E-null mice. FASEB Journal, 18(2), 418-420.

Short telomeres protect from diet-induced atherosclerosis in apolipoprotein E-null mice. / Poch, Enric; Carbonell, Paz; Franco, Sonia; Díez-Juan, Antonio; Blasco, María A.; Andrés, Vicente.

In: FASEB Journal, Vol. 18, No. 2, 2004, p. 418-420.

Research output: Contribution to journalArticle

Poch, E, Carbonell, P, Franco, S, Díez-Juan, A, Blasco, MA & Andrés, V 2004, 'Short telomeres protect from diet-induced atherosclerosis in apolipoprotein E-null mice.', FASEB Journal, vol. 18, no. 2, pp. 418-420.
Poch E, Carbonell P, Franco S, Díez-Juan A, Blasco MA, Andrés V. Short telomeres protect from diet-induced atherosclerosis in apolipoprotein E-null mice. FASEB Journal. 2004;18(2):418-420.
Poch, Enric ; Carbonell, Paz ; Franco, Sonia ; Díez-Juan, Antonio ; Blasco, María A. ; Andrés, Vicente. / Short telomeres protect from diet-induced atherosclerosis in apolipoprotein E-null mice. In: FASEB Journal. 2004 ; Vol. 18, No. 2. pp. 418-420.
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AU - Andrés, Vicente

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