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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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After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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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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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...
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Related Experiment Video

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Author Spotlight: Developing Parmodulins to Target Protease-Activated Receptors for Inflammation Control
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Proprotein convertases in atherogenesis.

Philipp Stawowy1

  • 1Deutsches Herzzentrum Berlin, Department of Medicine/Cardiology, Berlin, Germany.

Current Opinion in Lipidology
|June 24, 2015
PubMed
Summary

Proprotein convertases subtilisin/kexin (PCSKs) are key in cardiovascular diseases, impacting atherosclerosis and metabolic risk factors. Targeting PCSK9, a regulator of cholesterol, offers a promising therapeutic strategy for cardiovascular conditions.

Area of Science:

  • Biochemistry
  • Cardiology
  • Molecular Biology

Background:

  • Proprotein convertases subtilisin/kexin (PCSKs) are endoproteases involved in activating hormone and peptide precursors.
  • PCSKs are recognized as mediators in atherogenesis due to their diverse substrates and disease regulation.
  • The discovery of PCSK9's role in low-density lipoprotein receptor regulation has renewed interest in PCSKs for cardiovascular diseases.

Purpose of the Study:

  • To review the role of PCSKs in cardiovascular diseases.
  • To highlight the function of PCSK9 in regulating cholesterol and its impact on atherosclerosis.
  • To explore novel therapeutic strategies targeting PCSKs.

Main Methods:

  • Review of recent scientific data on PCSKs in atherosclerosis and cardiometabolic risk factors.

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  • Analysis of studies involving PCSK inhibition in animal models.
  • Examination of emerging anti-PCSK9 strategies like genome editing and vaccination.

    • Main Results:

    • PCSKs are expressed in human atheroma and regulated in atherosclerosis models.
    • PCSK inhibition reduces atherosclerosis by affecting cell proliferation, migration, and inflammation.
    • Targeting PCSK9 lowers cholesterol and reduces vascular lesion formation in mice.
    • PCSKs contribute to insulin resistance and obesity, key cardiometabolic risk factors.

    Conclusions:

    • PCSKs significantly influence cardiovascular diseases through atherosclerotic lesion formation and cardiometabolic risk factors.
    • PCSK9 is a critical regulator of plasma cholesterol, impacting atherosclerosis.
    • PCSK9 has emerged as a key pharmacological target for cardiovascular disease management.