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Updated: Apr 16, 2026

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Endothelin and endothelial dysfunction.

Tomoh Masaki1, Tatsuya Sawamura2

  • 1International Research and Educational Institute for Integrated Medical Sciences (IREIIMS), Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan . ; Recipient of the Japan Academy Prize in 1994.

Proceedings of the Japan Academy. Series B, Physical and Biological Sciences
|March 21, 2015
PubMed
Summary
This summary is machine-generated.

Endothelial dysfunction, an imbalance between nitric oxide (NO) and endothelin-1 (ET-1), is worsened by oxidized low-density lipoprotein (oxLDL) via the LOX-1 receptor. This pathway promotes cardiovascular disease progression.

Keywords:
Endothelial dysfunctionLOX-1endothelinendothelin receptorendothelin-converting enzymeoxLDL

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Area of Science:

  • Vascular biology
  • Cardiovascular research
  • Molecular medicine

Background:

  • Nitric oxide (NO) and endothelin (ET) are key regulators of vascular function.
  • An imbalance between NO and ET, termed endothelial dysfunction, is implicated in cardiovascular diseases.
  • Endothelin-1 (ET-1) is a potent vasoconstrictor and a significant factor in cardiovascular pathology.

Purpose of the Study:

  • To investigate the role of oxidized low-density lipoprotein (oxLDL) and its receptor LOX-1 in endothelial dysfunction.
  • To elucidate the molecular mechanisms linking LOX-1 activation to the NO/ET-1 imbalance.
  • To establish LOX-1 as a potential therapeutic target in cardiovascular diseases.

Main Methods:

  • Cloning and characterization of the endothelial oxLDL receptor, LOX-1.
  • Investigating the signaling pathways activated by LOX-1, including reactive oxygen species (ROS) and nuclear factor κB (NFκB).
  • Assessing the impact of LOX-1 activation on the expression of NO and ET-1 in endothelial cells.

Main Results:

  • Activation of LOX-1 by oxLDL leads to the generation of reactive oxygen species (ROS).
  • LOX-1 activation triggers the nuclear factor κB (NFκB) signaling pathway.
  • This results in decreased production of nitric oxide (NO) and increased production of endothelin-1 (ET-1), characteristic of endothelial dysfunction.
  • ET-1 exacerbates cardiovascular diseases in the context of endothelial dysfunction.

Conclusions:

  • LOX-1 is a critical mediator in the development of endothelial dysfunction.
  • The oxLDL-LOX-1 axis disrupts the NO/ET-1 balance, promoting a pro-atherogenic state.
  • Targeting LOX-1 may offer a novel therapeutic strategy for managing cardiovascular diseases associated with endothelial dysfunction.