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Related Experiment Video

Updated: Jun 12, 2025

Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification
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MARCH5 ameliorates aortic valve calcification via RACGAP1-DRP1 associated mitochondrial quality control.

Jialiang Zhang1, Yaoyu Zhang2, Wenhua Lei2

  • 1Laboratory of Cardiac Structure and Function, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, PR China; Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China; Cardiac Structure and Function Research Key Laboratory of Sichuan Province, West China Hospital, Sichuan University, Chengdu 610041, PR China.

Biochimica Et Biophysica Acta. Molecular Cell Research
|January 29, 2025
PubMed
Summary
This summary is machine-generated.

Mitochondrial E3 ubiquitin ligase MARCH5 deficiency impairs mitochondrial quality control, promoting aortic valve calcification by activating RACGAP1 and DRP1. Restoring MARCH5 or inhibiting RACGAP1 may offer therapeutic benefits.

Keywords:
Aortic valve calcificationDRP1MARCH5Mitochondrial quality controlOsteogenic differentiationRACGAP1

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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Biology
  • Cellular Stress Response

Background:

  • Mitochondrial E3 ubiquitin ligase (MARCH5) is crucial for mitochondrial function.
  • Aortic valve calcification (AVC) involves impaired mitochondrial quality control.
  • The specific role of MARCH5 in AVC pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the role and underlying mechanism of MARCH5 in aortic valve calcification.
  • To explore the relationship between MARCH5, mitochondrial dynamics, and osteogenic differentiation in valvular cells.

Main Methods:

  • Analyzed MARCH5 expression in human aortic valves.
  • Assessed mitochondrial morphology, osteogenic differentiation, and oxidative phosphorylation in human aortic valvular interstitial cells (HVICs).
  • Utilized MARCH5-knockdown and ApoE-knockout mouse models for in vivo studies.

Main Results:

  • MARCH5 protein levels were decreased in calcified valves, correlating with impaired mitochondrial quality control.
  • MARCH5 inhibition accelerated osteogenic transformation in HVICs, while overexpression had protective effects.
  • MARCH5 interacted with RACGAP1, promoting its ubiquitination and leading to DRP1 activation and mitochondrial dysfunction. Inhibiting RACGAP1 reversed MARCH5-silencing-induced calcification.

Conclusions:

  • Downregulation of MARCH5 promotes RACGAP1 ubiquitination and DRP1 activation, impairing mitochondrial quality control and contributing to aortic valve calcification.
  • MARCH5-RACGAP1-DRP1 axis represents a potential therapeutic target for aortic valve calcification.