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Related Experiment Video

Updated: Sep 7, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Ecklonia cava extracts decrease hypertension-related vascular calcification by modulating PGC-1α and SOD2.

Kyung-A Byun1, Seyeon Oh2, Jin Young Yang2

  • 1Department of Anatomy & Cell Biology, Gachon University College of Medicine, Incheon 21936, Republic of Korea; Functional Cellular Networks Laboratory, Lee Gil Ya Cancer and Diabetes Institute, Gachon University College of Medicine, Incheon 21999, Republic of Korea.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|June 19, 2022
PubMed
Summary
This summary is machine-generated.

Ecklonia cava extract (ECE) combats vascular calcification by boosting PGC-1α and SIRT3, enhancing SOD2 activity. This reduces mitochondrial damage and calcium deposition, protecting blood vessels in hypertension.

Keywords:
Ecklonia cava extractMitochondrial reactive oxygen speciesPeroxisome proliferator-activated receptor-gamma coactivator-1 alphaSirtuin-3Superoxide dismutase 2

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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Pharmacology

Background:

  • Vascular calcification (VC) involves mitochondrial dysfunction and VSMC transformation, linked to decreased SIRT3 and SOD2.
  • Hypertension exacerbates VC through increased mtROS and mitochondrial damage.

Purpose of the Study:

  • To investigate Ecklonia cava extract's (ECE) efficacy in mitigating VC.
  • To elucidate ECE's mechanism involving PGC-1α, SIRT3, and SOD2 in VSMCs.

Main Methods:

  • In vitro VSMC models treated with serum from WKY, SHR, and ECE-treated SHR rats.
  • In vivo studies using spontaneous hypertensive rat (SHR) models.
  • Analysis of PGC-1α, SIRT3, SOD2, mtROS, mtDNA damage, and mitochondrial dynamics.

Main Results:

  • ECE treatment increased PGC-1α, SIRT3 expression, and SOD2 activity, reducing mtROS and mtDNA damage in VSMCs.
  • ECE normalized mitochondrial dynamics (fusion, fission, mitophagy, biogenesis) and decreased NADPH oxidase activity and calcium deposition.
  • PGC-1α silencing abrogated the beneficial effects of ECE.

Conclusions:

  • ECE effectively reduces vascular calcification by upregulating PGC-1α and SIRT3, leading to enhanced SOD2 activity.
  • ECE protects against mitochondrial damage and dysfunction, thereby preventing VSMC phenotypic changes and calcification in hypertension.