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Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

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...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

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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Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
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Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

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 III: Management

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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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.

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A Calcium Phosphate-Induced Mouse Abdominal Aortic Aneurysm Model
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Published on: November 18, 2022

Calpain and atherosclerosis.

Takuro Miyazaki1, Takayuki Koya, Yasuyoshi Kigawa

  • 1Department of Biochemistry, Showa University School of Medicine, Tokyo 142-8555, Japan. taku@pharm.showa-u.ac.jp

Journal of Atherosclerosis and Thrombosis
|November 23, 2012
PubMed
Summary

Calpains, calcium-sensitive proteases, promote atherosclerosis by damaging blood vessels and impairing cholesterol regulation. Targeting calpains offers a potential strategy for controlling this cardiovascular disease.

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Area of Science:

  • Biochemistry
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Calpains are Ca(2+)-sensitive intracellular proteases with diverse cellular functions.
  • µ- and m-calpains are extensively characterized isozymes involved in vascular homeostasis.
  • Previous studies suggest calpains regulate nitric oxide production, endothelial barrier function, and angiogenesis.

Purpose of the Study:

  • To review the pro-atherogenic roles of calpains in the development of atherosclerosis.
  • To highlight the molecular mechanisms by which calpains contribute to vascular dysfunction and lipid metabolism.

Main Methods:

  • Review of existing literature on calpain function in vascular cells, macrophages, and hepatocytes.
  • Analysis of cell-based experiments demonstrating calpain involvement in LDL-induced endothelial dysfunction and foam cell formation.

Main Results:

  • Modified LDL-induced m-calpain causes endothelial hyperpermeability, facilitating lipid and monocyte infiltration.
  • Calpains mediate oxidized LDL-induced endothelial cell apoptosis.
  • In macrophages, calpains degrade ABCA1 and ABCG1, impairing cholesterol efflux and promoting foam cell formation.
  • Calpains may contribute to smooth muscle cell phenotype switching and disrupt high-density lipoprotein biogenesis in hepatocytes.

Conclusions:

  • Calpains play significant pro-atherogenic roles through multiple cellular mechanisms.
  • Targeting calpains represents a potential therapeutic strategy for atherosclerosis management.