Chlamydia pneumoniaeAlters Mildly Oxidized Low‐Density Lipoprotein–Induced Cell Death in Human Endothelial Cells, Leading to Necrosis Rather Than Apoptosis
Author(s) -
Dani Nazzal,
AnneValérie Cantéro,
Nicole Therville,
Bruno Ségui,
Anne NègreSalvayre,
Mogens Thomsen,
Hervé Benoist
Publication year - 2005
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/498617
Subject(s) - apoptosis , programmed cell death , fragmentation (computing) , biology , dna fragmentation , necrosis , reactive oxygen species , cytochrome c , oxidative stress , poly adp ribose polymerase , microbiology and biotechnology , biochemistry , polymerase , dna , ecology , genetics
Atherosclerosis is characterized by oxidative stress that induces lipid and protein oxidation in the vascular wall. Oxidized low-density lipoproteins (oxLDLs) are present in lesions, and one of their actions is to induce apoptosis or necrosis in vascular cells. A role for Chlamydia pneumoniae in atherosclerosis has been proposed, but the mechanisms involved remain largely unknown.
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