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Protein tyrosine nitration in atherosclerotic endothelial dysfunction.

Miao Jiang1, Xiao-Mei Zhao2, Zhi-Sheng Jiang3

  • 1Institute of Cardiovascular Disease, Department of Pathophysiology, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Postdoctoral Research Station of Basic Medicine, University of South China, Hengyang 421001, China; Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, Bioengineering Collage of Chongqing University, Chongqing 400030, China.

Clinica Chimica Acta; International Journal of Clinical Chemistry
|February 12, 2022
PubMed
Summary

Reactive oxygen species (ROS) cause protein tyrosine nitration and endothelial dysfunction in atherosclerosis. Protein tyrosine nitration may be a cause of endothelial dysfunction, offering insights into atherosclerosis mechanisms.

Keywords:
AtherosclerosisCardiovascular diseaseEndothelial dysfunctionProtein tyrosine nitrationROS/RNS

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Area of Science:

  • Biochemistry
  • Cardiovascular Biology
  • Pathophysiology

Background:

  • Reactive oxygen species (ROS) accumulation contributes to atherosclerosis.
  • Endothelial dysfunction, characterized by impaired vasorelaxation, is linked to nitric oxide (NO) imbalance.
  • ROS-mediated peroxynitrite formation reduces NO bioavailability and promotes protein tyrosine nitration.

Purpose of the Study:

  • To review the process and implications of protein tyrosine nitration.
  • To explore the association between nitrated proteins and endothelial dysfunction in cardiovascular disease.
  • To investigate the role of tyrosine nitration in the mechanisms of endothelial dysfunction.

Main Methods:

  • Literature review of studies on protein tyrosine nitration and endothelial dysfunction.
  • Analysis of the biochemical pathways involving ROS, NO, and peroxynitrite.
  • Examination of evidence linking nitrated proteins to cardiovascular disease.

Main Results:

  • Protein tyrosine nitration is increased in cardiovascular disease.
  • Nitration alters protein structure and function, contributing to endothelial dysfunction.
  • Tyrosine nitration can interfere with antioxidant defenses.

Conclusions:

  • Protein tyrosine nitration is implicated as a cause of endothelial dysfunction.
  • Understanding nitration mechanisms provides insights into atherosclerosis.
  • Targeting protein tyrosine nitration may offer therapeutic strategies for endothelial dysfunction.