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Updated: Feb 28, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
[Sirt1 inhibited oxidized low-density lipoprotein induced smooth muscle cells inflammatory response]
1Department of Cardiovascular, Yunnan Provincial Corps Hospital, Chinese People's Armed Police Force, Kunming 650111, China.
Abstract:
Objective: To investigate the mechanism of inflammation of smooth muscle cells induced by oxidized low-density lipoprotein through Sirt1 in the atherosclerosis. Methods: The expression of Sirt1 had been measured in the plaque tissues of human and mice. The affection of overexpression of SIRT1 on the oxLDL induced-inflammatory response and ROS generation had been detected in this study. Results: Sirt1 decreased in smooth muscle cells region of human plaque. And in the smooth muscle cells region of mice plaque, Sirt1 was also significantly decreased about 5-fold (P<0.05). Although, oxLDL promoted inflammatory cytokines secretion and ROS generation, but this affection had been reversed by upregulating Sirt1. Conclusion: oxLDL regulated smooth muscle cells inflammatory response via Sirt1. Thus, Sirt1 is a signaling molecular regulating smooth muscles inflammatory response in the process of atherosclerosis.
Insights
Oxidized low-density lipoprotein (oxLDL) promotes inflammation in atherosclerosis by decreasing Sirt1 in smooth muscle cells. Upregulating Sirt1 reverses this inflammatory response, highlighting its role in the disease.
Area of Science:
- Cardiovascular Biology
- Molecular Mechanisms of Atherosclerosis
- Cellular Inflammation
Background:
- Atherosclerosis involves inflammation of smooth muscle cells.
- Oxidized low-density lipoprotein (oxLDL) is implicated in atherosclerotic plaque development.
- The role of Sirtuin 1 (Sirt1) in oxLDL-induced smooth muscle cell inflammation requires elucidation.
Purpose of the Study:
- To investigate the mechanism by which oxLDL induces smooth muscle cell inflammation via Sirt1.
- To determine the expression levels of Sirt1 in atherosclerotic plaques.
- To assess the impact of Sirt1 modulation on oxLDL-induced inflammatory responses and reactive oxygen species (ROS) generation.
Main Methods:
- Quantified Sirt1 expression in human and mouse atherosclerotic plaque tissues.
- Utilized overexpression of Sirt1 in smooth muscle cells.
- Measured inflammatory cytokine secretion and ROS generation in response to oxLDL and Sirt1 modulation.
Main Results:
- Sirt1 expression was significantly decreased in the smooth muscle cell regions of human and mouse atherosclerotic plaques.
- Oxidized low-density lipoprotein (oxLDL) exposure increased inflammatory cytokine secretion and ROS generation.
- Upregulation of Sirt1 reversed the pro-inflammatory and pro-oxidative effects of oxLDL.
Conclusions:
- Oxidized low-density lipoprotein (oxLDL) regulates smooth muscle cell inflammatory responses through Sirt1.
- Sirt1 acts as a key signaling molecule in modulating smooth muscle cell inflammation during atherosclerosis.
- Targeting Sirt1 may offer a therapeutic strategy for atherosclerosis.
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