Extracellular peroxiredoxin 5 exacerbates atherosclerosis via the TLR4/MyD88 pathway.
Document Type
Article
Publication Date
1-1-2025
Publication Title
Atherosclerosis
Keywords
JGM, Peroxiredoxins, Animals, Toll-Like Receptor 4, Atherosclerosis, Humans, Myeloid Differentiation Factor 88, Human Umbilical Vein Endothelial Cells, Signal Transduction, Lipoproteins, LDL, Mice, Knockout, ApoE, Mice, Disease Models, Animal, Mice, Inbred C57BL, Male, Plaque, Atherosclerotic, Oxidative Stress, Mice, Knockout, Apolipoproteins E, Cell Movement
JAX Source
Atherosclerosis. 2024;400:119052.
Volume
400
First Page
119052
Last Page
119052
ISSN
1879-1484
PMID
39549462
DOI
https://doi.org/10.1016/j.atherosclerosis.2024.119052
Abstract
BACKGROUNGD AND AIMS: Peroxiredoxin 5 (PRDX5), an atypical 2-Cys peroxiredoxin (PRDX), is known to regulate global oxidative stresses and inflammatory responses. Inflammation and oxidative stress are pivotal factors in the development of atherosclerosis, especially in the context of vascular endothelial dysfunction. However, effects of PRDX5 on atherosclerosis remain unclear. This study aimed to elucidate the role of PRDX5 in the pathogenesis of atherosclerosis.
METHODS: For in vivo analysis, normal chow diet 60-week old Apolipoprotein E knockout (ApoE
RESULTS: We observed elevated PRDX5 expression under atherosclerotic conditions in both humans and mice. Unexpectedly, Prdx5
CONCLUSIONS: These data demonstrate that extracellular PRDX5 contributes to endothelial inflammation, promoting macrophage accumulation in the atherosclerotic aorta through activation of TLR4/MyD88/NF-κB and P38 signaling pathways, thereby exacerbating the progression of atherosclerosis.
Recommended Citation
Kweon H,
Song E,
Jeong S,
Lee S,
Sonn S,
Seo S,
Jin J,
Kim S,
Kim T,
Moon S,
Kim D,
Park Y,
Woo H,
Oh G.
Extracellular peroxiredoxin 5 exacerbates atherosclerosis via the TLR4/MyD88 pathway. Atherosclerosis. 2024;400:119052.