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Assessment of Vascular Function in Patients With Chronic Kidney Disease
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Not all vascular smooth muscle cell exosomes calcify equally in chronic kidney disease

Adriana Dusso1, Maria Isabel Colombo2, Catherine M Shanahan3

  • 1Bone and Mineral Research Unit, Hospital Universitario Central de Asturias, Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.

Kidney International
|February 2, 2018
PubMed

Insights

Vascular smooth muscle cells in chronic kidney disease release microvesicles that worsen medial calcification. Understanding exosome regulation is key to blocking this harmful cell communication and preventing vascular disease.

Area of Science:

  • Cardiovascular Biology
  • Cell Biology
  • Nephrology

Background:

  • Medial calcification in chronic kidney disease (CKD) threatens vascular smooth muscle cell (VSMC) health.
  • CKD-induced stress prompts VSMCs to increase exosome release, exacerbating pathological calcification.

Purpose of the Study:

  • To review the mechanisms of microvesicle/exosome biogenesis and secretion.
  • To inform strategies for inhibiting procalcifying intercellular communication in CKD.

Main Methods:

  • Literature review on microvesicle/exosome regulation.
  • Analysis of cell-to-cell communication in pathological calcification.

Main Results:

  • Calcifying VSMCs release microvesicles that transmit procalcifying signals to normal VSMCs.
  • Exosome formation and release are increased by VSMCs under CKD stress.

Conclusions:

  • Microvesicles play a critical role in propagating calcifying signals between VSMCs.
  • Targeting microvesicle biogenesis and secretion is a potential therapeutic strategy for CKD-related vascular calcification.

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