LDR-adapted liver-derived cytokines have potential to induce atherosclerosis.
Eunguk ShinDahye KimYou Yeon ChoiHyeSook YounKi Moon SeongBuHyun YounPublished in: International journal of radiation biology (2022)
After irradiation with LDR (100 mGy) the mice showed atherosclerotic phenotypes and through analysis results, we selected regulated cytokines, PAI-1 and AR, and found that these were changed in the liver. LDR-regulated cytokines have the potential to be transported to endothelial cells and induce lipid accumulation, inflammation of monocytes, increased oxidized low-density lipoprotein (oxLDL) and foam cells formation, that were series of phenotypes lead to plaque formation in endothelial cells and induces atherosclerosis. As a further aspect of this study, testosterone undecanoate (TU) was found to pharmacologically inhibit a series of atherosclerotic phenotypes exhibited by LDR. This study suggests a role for PAI-1 and AR in regulating the development of atherosclerosis after LDR exposure. Targeting PAI-1 and AR could serve as an attractive strategy for the management of atherosclerosis following LDR exposure.
Keyphrases
- endothelial cells
- cardiovascular disease
- low density lipoprotein
- induced apoptosis
- oxidative stress
- type diabetes
- coronary artery disease
- endoplasmic reticulum stress
- immune response
- adipose tissue
- high glucose
- cell cycle arrest
- dendritic cells
- skeletal muscle
- radiation therapy
- insulin resistance
- cell proliferation
- cancer therapy
- risk assessment
- climate change
- cell death
- peripheral blood
- replacement therapy
- pi k akt