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Transducer Mechanism: Enzyme-Linked Receptors01:27

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Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
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Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
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Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

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Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
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Related Experiment Video

Updated: Oct 18, 2025

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
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ANGPTL3 as therapeutic target.

Sander Kersten1

  • 1Nutrition, Metabolism and Genomics Group, Division of Human Nutrition and Health, Wageningen University, the Netherlands.

Current Opinion in Lipidology
|September 28, 2021
PubMed
Summary

Inactivating ANGPTL3, a key factor in lipid metabolism, effectively lowers LDL-C and triglycerides. This offers a promising new approach for managing atherosclerotic cardiovascular disease risk.

Area of Science:

  • Biochemistry
  • Genetics
  • Cardiology

Background:

  • Elevated LDL-C and triglycerides are significant risk factors for atherosclerotic cardiovascular disease.
  • Current lipid-lowering therapies often fail to achieve target levels for many patients.
  • ANGPTL3 has emerged as a novel therapeutic target for managing dyslipidemia.

Purpose of the Study:

  • To provide an overview of recent literature on ANGPTL3.
  • To focus on the therapeutic benefits of ANGPTL3 inactivation.
  • To discuss potential mechanisms of ANGPTL3's lipid-lowering effects.

Main Methods:

  • Review of recent literature on ANGPTL3.
  • Focus on therapeutic benefits of ANGPTL3 inactivation via monoclonal antibodies and antisense oligonucleotides.

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  • Discussion of emerging therapeutic approaches targeting ANGPTL3.
  • Main Results:

    • ANGPTL3, secreted by the liver, inhibits lipases by complexing with ANGPTL8.
    • Loss-of-function variants in ANGPTL3 are associated with lower LDL-C, triglycerides, and reduced cardiovascular risk.
    • Clinical studies show ANGPTL3 inactivation significantly lowers LDL-C and triglycerides in dyslipidemia patients.

    Conclusions:

    • Anti-ANGPTL3 therapies demonstrate significant potential for reducing LDL-C and triglycerides.
    • These therapies are promising for selected patient groups with dyslipidemia.
    • Targeting ANGPTL3 represents a novel strategy in cardiovascular disease prevention.