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Related Concept Videos

Atherosclerosis I: Introduction01:30

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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Understanding serum lipids is crucial for maintaining cardiovascular health and preventing heart disease and stroke.
Serum lipids are fats and fatty substances in the blood and are crucial for various bodily functions, including energy storage, cellular structure, and hormone production. Serum lipids consist of cholesterol, triglycerides, and phospholipids.
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Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
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Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
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Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Inflammatory Links Between Hypertriglyceridemia and Atherogenesis.

Xueying Peng1, Huaizhu Wu2

  • 1Department of Clinical Pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310006, People's Republic of China. pengxy1991@126.com.

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Summary

High triglyceride levels (hypertriglyceridemia) are linked to heart disease. Understanding how high triglycerides cause atherosclerosis and the role of inflammation is key to developing new therapies for cardiovascular disease prevention.

Keywords:
Atherosclerotic cardiovascular disease (ASCVD)Hypertriglyceridemia (HTG)InflammationRemnant lipoprotein particles (RLP)Triglyceride-rich lipoproteins (TGRL)

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Area of Science:

  • Cardiovascular Science
  • Metabolic Disorders
  • Inflammation Research

Background:

  • Hypertriglyceridemia (HTG), characterized by elevated triglyceride-rich lipoproteins (TGRL), is increasingly recognized as a causal risk factor for atherosclerotic cardiovascular disease (ASCVD).
  • The precise mechanisms linking HTG to ASCVD remain incompletely elucidated but involve complex interactions with inflammatory pathways.
  • Triglyceride-rich lipoproteins and their remnants may play a more significant role in promoting inflammation and atherogenesis compared to low-density lipoproteins.

Purpose of the Study:

  • To review the potential mechanisms connecting hypertriglyceridemia (HTG) and atherosclerotic cardiovascular disease (ASCVD) risk.
  • To discuss the potential efficacy of therapies targeting HTG in the prevention of ASCVD.

Main Methods:

  • This review synthesizes current clinical and preclinical evidence.
  • It examines the role of inflammation in the atherogenic process associated with HTG.
  • It evaluates emerging therapeutic strategies for HTG and inflammation.

Main Results:

  • Elevated TGRL and their remnants contribute to ASCVD by penetrating the endothelium, promoting macrophage foam cell formation, and driving arterial wall inflammation.
  • Lipid-laden foamy monocytes, derived from TGRL uptake, may infiltrate the arterial wall, further contributing to atherogenesis.
  • Inflammation is a critical mediator in the causal relationship between HTG and ASCVD.

Conclusions:

  • Hypertriglyceridemia (HTG) is a significant risk factor for atherosclerotic cardiovascular disease (ASCVD), with inflammation playing a central role in its pathogenesis.
  • Novel therapeutic interventions targeting HTG and/or inflammation show promise in reducing the residual ASCVD risk associated with elevated triglyceride levels.