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Related Experiment Video

Updated: Nov 8, 2025

Visualization of Vascular Ca2+ Signaling Triggered by Paracrine Derived ROS
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Oxidative stress in vascular calcification.

Chu-Ting Hu1, Yi-Duo Shao2, Yi-Zhang Liu3

  • 1Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Research Lab for Clinical & Translational Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Departments of Medical Laboratory, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China.

Clinica Chimica Acta; International Journal of Clinical Chemistry
|April 22, 2021
PubMed
Summary
This summary is machine-generated.

Oxidative stress (OS) significantly drives vascular calcification (VC) by affecting phosphate balance, cell differentiation, and inflammation. Antioxidants show promise for treating VC, a condition linked to high mortality in cardiovascular disease, chronic kidney disease, and diabetes.

Keywords:
AntioxidantsInflammationOxidative stressReactive oxygen speciesVascular calcification

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Area of Science:

  • Biomedical Science
  • Cardiovascular Research
  • Renal Medicine

Background:

  • Vascular calcification (VC) is a hallmark of cardiovascular disease (CVD), chronic kidney disease (CKD), and diabetes, contributing to significant mortality.
  • The precise role of oxidative stress (OS) in the development and progression of VC remains incompletely understood.
  • Key enzymes like NADPH oxidases, MPO, NOSs, SOD, and PONs are implicated in reactive oxygen species (ROS) production and OS.

Purpose of the Study:

  • To elucidate the impact of oxidative stress (OS) on the mechanisms underlying vascular calcification (VC).
  • To explore the potential of antioxidant therapies in managing VC.

Main Methods:

  • Review of literature on enzymes involved in ROS production (NADPH oxidases, xanthine oxidases, MPO, NOSs, SOD, PONs).
  • Analysis of established mechanisms linking OS to VC, including phosphate balance, VSMC differentiation, inflammation, DNA damage, and ECM remodeling.

Main Results:

  • Excess ROS-induced OS is identified as a critical mediator in promoting VC.
  • OS influences multiple pathways crucial to VC pathogenesis, such as regulating phosphate homeostasis and vascular smooth muscle cell (VSMC) phenotype.
  • Inflammation, DNA damage, and extracellular matrix (ECM) remodeling are significantly impacted by OS in the context of VC.

Conclusions:

  • Oxidative stress is a significant regulator of vascular calcification.
  • Antioxidant strategies represent a promising therapeutic avenue for mitigating VC and its associated mortality.