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Related Concept Videos

Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

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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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Triglycerides serve as crucial long-term energy storage molecules in microorganisms, providing a dense source of metabolic energy. Their breakdown is mediated by lipases, which hydrolyze triglycerides into glycerol and free fatty acids. Each of these components follows distinct metabolic pathways, ultimately contributing to ATP synthesis and cellular energy homeostasis.Glycerol MetabolismGlycerol, released from triglyceride hydrolysis, is phosphorylated by glycerol kinase to form...
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Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
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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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Atherosclerosis III: Management01:26

Atherosclerosis III: Management

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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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Lipids are large molecules that are generally not water-soluble. Since most of the digestive enzymes in the human body are water-based, there are specific steps the body must take to break down lipids and make them available for use.
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Related Experiment Video

Updated: Sep 9, 2025

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
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Familial Hypercholesterolemia: Still an Enigma.

Sahej Arora1, Adnan Kharsa2, Gaurav Sharma2

  • 1Department of Internal Medicine, Rochester General Hospital, Rochester, New York, USA.

JACC. Case Reports
|August 29, 2025
PubMed
Summary

Familial hypercholesterolemia (FH) is a genetic disorder causing high LDL cholesterol. Remarkably, some patients with FH may not develop atherosclerosis, suggesting protective factors influencing lipid metabolism.

Keywords:
atherosclerosiscardiovascular preventionfamilial hypercholesterolemiastatins

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Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Metabolic Disorders

Background:

  • Familial hypercholesterolemia (FH) is an inherited condition.
  • Characterized by significantly elevated low-density lipoprotein (LDL) cholesterol levels.
  • Associated with premature atherosclerotic cardiovascular disease.

Observation:

  • A 61-year-old woman with a decade-long history of LDL >200 mg/dL was diagnosed with FH.
  • She carried a pathogenic LDLR mutation.
  • Risk stratification revealed no evidence of atherosclerotic disease via coronary CT angiography or carotid ultrasound.

Findings:

  • Despite lifelong severe hypercholesterolemia and a pathogenic LDLR mutation, the patient showed no signs of atherosclerosis.
  • Coronary artery calcifications typically appear early in FH patients (11-23 years).
  • The absence of cardiovascular disease and family history suggested a potential protective factor in her LDL metabolism.

Implications:

  • Heterozygous FH patients can remain free of atherosclerosis.
  • This case highlights potential protective mechanisms against hyperlipidemia-induced cardiovascular disease.
  • Further research into these protective factors could offer novel therapeutic targets for FH.