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Endothelial dysfunction after repeated Chlamydia pneumoniae infection in apolipoprotein E-knockout mice.

Authors
  • Liuba, P
  • Karnani, P
  • Pesonen, E
  • Paakkari, I
  • Forslid, A
  • Johansson, L
  • Persson, K
  • Wadström, T
  • Laurini, R
Type
Published Article
Journal
Circulation
Publisher
Ovid Technologies Wolters Kluwer -American Heart Association
Publication Date
Aug 29, 2000
Volume
102
Issue
9
Pages
1039–1044
Identifiers
PMID: 10961970
Source
Medline
License
Unknown

Abstract

C pneumoniae impairs arterial endothelial function, and the NO pathway is principally involved. Cyclooxygenase-dependent vasoconstricting products may also account for the infection-induced impaired relaxation. These findings further support the role of C pneumoniae infection in atherosclerosis development.

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