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Published on: January 13, 2012
The more critical murderer of atherosclerosis than lipid metabolism: chronic stress
Ling-Bing Meng1, Ruomei Qi2, Lei Xu1
1Neurology Department, Beijing Hospital, National Center of Gerontology, No.1 Dahua Road, Dong Dan, Beijing, 100730, People's Republic of China.
Insights
Chronic stress (CS) is the primary independent risk factor for atherosclerosis, significantly impacting intimal and media thickness. This contrasts with low-density lipoprotein cholesterol (LDLC) and total cholesterol (TC), which showed no independent effect in this study.
Area of Science:
- Cardiovascular Research
- Atherosclerosis Pathophysiology
- Neuroscience
Background:
- Atherosclerotic cerebrovascular disease mortality is increasing, with intimal and media thickening as key contributors to cerebral ischemia.
- Low-density lipoprotein cholesterol (LDLC), total cholesterol (TC), and chronic stress (CS) are known atherosclerosis (AS) risk factors, but the leading independent factor remains unclear.
- Understanding the primary drivers of AS and its impact on vascular thickness is crucial for public health.
Purpose of the Study:
- To investigate the independent effects of chronic stress (CS), LDLC, and TC on atherosclerosis (AS) and intimal-media thickness.
- To identify the principal independent risk factor contributing to AS development and progression.
- To analyze the associated histocyte mechanisms involving macrophages and endothelial cells.
Main Methods:
- Comparative analysis of normal, high-fat diet (HF), and HF plus CS conditions.
- Statistical analyses including χ2, Spearman's rho, multiple linear regression, and univariate Cox regression.
- Histological examination using immunohistochemistry to assess macrophagocytes and endotheliocytes in affected tissues.
Main Results:
- CS, LDLC, and TC were correlated with intimal-media thickness (P < 0.05) in initial analyses.
- Multiple linear regression identified CS as the sole independent risk factor for thickness (P < 0.05); LDLC and TC were not independent predictors.
- CS was linked to poorer non-depression time (NDT), and histological analysis revealed disordered endothelial cell arrangement under CS.
Conclusions:
- Chronic stress (CS) is identified as the primary independent risk factor for atherosclerosis and intimal-media thickness.
- LDLC and TC are not independent risk factors for AS or vascular thickness in the context of chronic stress.
- CS significantly impacts vascular structure and function, highlighting its critical role in cerebrovascular disease.
Background:
The mortality of atherosclerotic cerebrovascular disease is on the rise, and changes in intimal and media thickness are a leading cause of cerebral ischemia-related death. Levels of low density lipoprotein cholesterol (LDLC), total cholesterol (TC), and chronic stress (CS) are all recognized risk factors for atherosclerosis (AS). However, the leading independent risk factor is indistinct. This study explored the effects of chronic stress, LDLC, and TC on AS and intimal and media thickness, preliminarily explored the main risk factor of AS, and analyzed the related histocyte mechanisms for macrophages and endothelial cells.
Methods:
Conditions include normal, high-fat diet (HF), and HF plus CS. The correlations between intimal and media thickness and general risk factors were analyzed using χ2, Spearman's rho test, and multiple linear regression. Univariate Cox regression was used to identify potential factors that affect the non-depression time (NDT). We performed a ROC curve to determine the ability of this condition to predict the thickness. Immunohistochemistry was implemented to detect macrophagocytes and endotheliocytes.
Results:
Based on χ2 and Spearman's rho test, LDLC, TC, and CS are all related with intimal and media thickness (P < 0.05). However, in multiple linear regression, CS is still a risk factor of thickness (P < 0.05) but LDLC and TC are not. High levels of LDLC, TC, and CS were correlated with poor NDT (P < 0.05). This condition can predict the thickness sensitively. The endarterium is richest in macrophagocytes, and the arrangement of endotheliocytes is disordered and cracked under CS.
Conclusion:
CS is the main independent risk factor for AS and intimal (and media) thickness, rather than LDLC or TC.
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