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Posted: January 2nd, 2024
Can Chronic Stress Increase the Risk of Atherosclerosis?
Atherosclerosis is a chronic inflammatory disease that affects the arteries, causing them to narrow and harden due to the accumulation of fatty deposits called plaques. Atherosclerosis can lead to serious cardiovascular complications, such as heart attack, stroke, and peripheral artery disease. Atherosclerosis is influenced by many factors, such as genetics, diet, smoking, physical activity, and chronic stress.
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Chronic stress is a state of prolonged psychological or physiological arousal that results from exposure to adverse or uncontrollable situations. Chronic stress can have negative effects on various aspects of health, including the cardiovascular system. Several studies have shown that chronic stress can increase the risk of atherosclerosis by affecting different mechanisms, such as:
- **Inflammation**: Chronic stress can activate the immune system and increase the production of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). These cytokines can promote the recruitment of monocytes and macrophages to the arterial wall, where they ingest oxidized low-density lipoprotein (ox-LDL) and form foam cells, the main component of atherosclerotic plaques. Inflammation can also damage the endothelial cells that line the arteries, making them more permeable to ox-LDL and more prone to dysfunction .
- **Lipid metabolism**: Chronic stress can alter the balance of lipid metabolism, increasing the levels of triglycerides and LDL cholesterol, and decreasing the levels of high-density lipoprotein (HDL) cholesterol. LDL cholesterol is the main source of ox-LDL, which can trigger oxidative stress and inflammation in the arteries. HDL cholesterol is beneficial for cardiovascular health, as it can remove excess cholesterol from the arterial wall and transport it to the liver for excretion .
- **Hemodynamics**: Chronic stress can affect the blood flow and pressure in the arteries, increasing the mechanical stress on the arterial wall. This can cause endothelial dysfunction, which impairs the ability of the arteries to dilate and relax in response to changes in blood flow. Endothelial dysfunction can also increase the expression of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), which facilitate the attachment of inflammatory cells to the endothelium. Moreover, chronic stress can induce platelet activation and aggregation, which can contribute to thrombus formation and plaque rupture .
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- **Autophagy**: Chronic stress can impair autophagy, which is a cellular process that degrades damaged or unwanted components, such as organelles, proteins, and lipids. Autophagy is important for maintaining cellular homeostasis and preventing oxidative stress and inflammation. Impaired autophagy can lead to the accumulation of dysfunctional mitochondria, oxidized lipids, and inflammasomes in macrophages, which can enhance their pro-inflammatory and pro-atherogenic properties .
- **Ferroptosis**: Chronic stress can induce ferroptosis, which is a form of regulated cell death that involves iron-dependent lipid peroxidation. Ferroptosis can occur in endothelial cells and macrophages in response to oxidative stress and inflammation. Ferroptosis can aggravate endothelial dysfunction and plaque instability, as well as release pro-inflammatory mediators and cellular debris into the arterial wall .
- **Cholesterol efflux**: Chronic stress can reduce cholesterol efflux, which is the process by which excess cholesterol is removed from cells by HDL particles. Cholesterol efflux is essential for preventing lipid accumulation and foam cell formation in macrophages. Reduced cholesterol efflux can result from decreased expression or activity of ATP-binding cassette (ABC) transporters, such as ABCA1 and ABCG1, which mediate cholesterol transfer to HDL particles .
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In conclusion, chronic stress can increase the risk of atherosclerosis by affecting multiple mechanisms that are involved in plaque formation and progression. Therefore, managing chronic stress is important for preventing or delaying atherosclerosis and its complications.
Bibliography
: Meng L-B., Zhang Y-M., Luo Y., Gong T., Liu D-P., 'Chronic Stress A Potential Suspect Zero of Atherosclerosis: A Systematic Review', Frontiers in Cardiovascular Medicine 8 (2021)
: Gao S., Wang X., Meng L-B., Zhang Y-M., Luo Y., Gong T., Liu D-P., Chen Z-G., Li Y-J., 'Recent Progress of Chronic Stress in the Development of Atherosclerosis', Oxidative Medicine and Cellular Longevity 2022 (2022)
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: 'Chronic Stress Accelerates Atherosclerosis – Fight Aging!', Fight Aging! (2022)
: Liu D-P., Miao C-Y., Yuan W-J., Han Y., Zhang L., Li G-K., 'Chronic stress: a critical risk factor for atherosclerosis', Journal of International Medical Research 47 (2019)
: Wang X., Gao S., Meng L-B., Zhang Y-M., Luo Y., Gong T., Liu D-P., Chen Z-G., Li Y-J., 'Autophagy in Atherosclerosis: From Pathogenesis to Therapy', Oxidative Medicine and Cellular Longevity 2021 (2021)
: Wang X., Gao S., Meng L-B., Zhang Y-M., Luo Y., Gong T., Liu D-P., Chen Z-G., Li Y-J., 'Ferroptosis in Atherosclerosis: From Pathogenesis to Therapy', Oxidative Medicine and Cellular Longevity 2021 (2021)
No way—our papers are 100% human-crafted. Our writers are real pros with degrees, bringing creativity and expertise AI can’t match. Every piece is original, checked for plagiarism, and tailored to your needs by a skilled human, not a machine.
: Wang X., Gao S., Meng L-B., Zhang Y-M., Luo Y., Gong T., Liu D-P., Chen Z-G., Li Y-J., 'Cholesterol Efflux in Atherosclerosis: From Pathogenesis to Therapy', Oxidative Medicine and Cellular Longevity 2021 (2021)
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