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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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DDR1 Regulates Femoral Arterial Calcification in Lower-Extremity Artery Disease Through NF-Kappa B Activation

Manovriti Thakur1,2, Thibaut Quillard3, Nico Angliker1,2

  • 1Division of Angiology, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.

Acta Physiologica (Oxford, England)
|December 16, 2025
PubMed

Insights

This study identifies DDR1 as a key driver of medial arterial calcification (MAC) in lower-extremity arterial disease (LEAD). Targeting DDR1 may offer a novel therapeutic approach to prevent MAC in LEAD patients.

Area of Science:

  • Vascular Biology
  • Cardiovascular Disease Research
  • Molecular Medicine

Background:

  • Lower-extremity arterial disease (LEAD) affects 230 million globally, with medial arterial calcification (MAC) common in patients and linked to mortality.
  • Current therapeutic strategies for femoral MAC in LEAD are lacking, and its underlying mechanisms require elucidation.
  • Understanding the molecular drivers of femoral MAC is crucial for developing targeted treatments.

Purpose of the Study:

  • To identify molecular drivers of femoral medial arterial calcification (MAC) in patients with lower-extremity arterial disease (LEAD).

Main Methods:

  • Analysis of human patient samples using von Kossa staining, immunofluorescence, and gene expression.
  • Assessment of medial calcification in Apoe-/- mice fed a Western diet (WD).
  • In vitro experiments with murine and human vascular smooth muscle cells (VSMCs) to evaluate DDR1's role in calcification.

Main Results:

  • Femoral arteries showed significantly higher calcification and pro-calcifying gene expression (DDR1, BMP2) compared to carotids.
  • DDR1 expression positively correlated with calcification in human femoral samples.
  • DDR1 inhibition reduced, while activation increased, calcium deposition in VSMCs; DDR1 stimulation activated NF-κB, a pathway implicated in calcification.

Conclusions:

  • DDR1 is identified as a key molecular driver of calcification in LEAD, operating via NF-κB activation.
  • Targeting DDR1 presents a potential novel therapeutic strategy for preventing medial arterial calcification in LEAD.
  • Further research into DDR1 inhibition could lead to new treatments for atherosclerotic cardiovascular disease manifestations.
Abstract

Keywords:
DDR1LEAD‐specific calcificationfemoral vascular smooth muscle cellmedial arterial calcification

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