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Related Experiment Video

Updated: Jan 18, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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GRP75 inhibition attenuates arterial calcification.

Jonas Heyn1, Andrea Gorgels1, Nicolas Hense1

  • 1Department of Internal Medicine I - Cardiology, Medical Faculty, Uniklinik RWTH Aachen, RWTH Aachen University, 52074, Aachen, Germany.

Atherosclerosis
|May 23, 2025
PubMed
Summary

Glucose-regulated protein 75 (GRP75) links mitochondria and endoplasmic reticulum (ER) in vascular smooth muscle cells (SMCs). Inhibiting GRP75 reduces arterial calcification by improving mitochondrial function and decreasing ER stress.

Keywords:
Arterial calcificationExtracellular vesiclesMitochondria-ER contactsMitochondria-associated membranesVascular smooth muscle cells

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Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Mitochondrial Biology

Background:

  • Arterial calcification, a risk factor for cardiovascular mortality, involves vascular smooth muscle cell (SMC) osteogenic transition.
  • Mitochondria-associated membranes (MAMs), contacts between mitochondria and the endoplasmic reticulum (ER), are implicated but their role in calcification is unknown.
  • Glucose-regulated protein 75 (GRP75) is a key protein linking MAMs.

Purpose of the Study:

  • To investigate the role of GRP75 and MAMs in SMC calcification.
  • To determine if GRP75 influences extracellular vesicle (EV) cargo in calcifying SMCs.

Main Methods:

  • Human coronary artery SMCs were cultured in osteogenic medium.
  • Mitochondria-associated membranes (MAMs) were isolated and visualized via electron microscopy.
  • GRP75 was inhibited using silencing RNA or MKT-077.
  • Mitochondrial respiration and ER stress were assessed.
  • SMC-derived EVs were isolated and analyzed.

Main Results:

  • Calcifying SMCs showed increased GRP75 expression and enhanced mitochondria-ER contacts.
  • GRP75 inhibition reduced matrix mineralization, attenuated mitochondria-ER contacts, and impaired mitochondrial respiration.
  • GRP75 was found to be enriched in EVs released by calcifying SMCs.

Conclusions:

  • Mitochondria-associated membranes (MAMs) are altered in calcifying SMCs.
  • GRP75 inhibition disrupts mitochondria-ER contacts, improves mitochondrial function, and reduces vascular calcification.
  • GRP75 represents a potential therapeutic target for preventing arterial calcification.