Store-operated calcium entry in thrombosis and thrombo-inflammation

Elmina Mammadova-Bach, Magdolna Nagy, Johan W. M. Heemskerk, Bernhard Nieswandt*, Attila Braun*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

28 Citations (Web of Science)

Abstract

Cytosolic free calcium (Ca2+) is a second messenger regulating a wide variety of functions in blood cells, including adhesion, activation, proliferation and migration. Store-operated Ca2+ entry (SOCE), triggered by depletion of Ca2+ from the endoplasmic reticulum, provides a main mechanism of regulated Ca2+ influx in blood cells. SOCE is mediated and regulated by isoforms of the ion channel proteins ORAI and TRP, and the transmembrane Ca2+ sensors stromal interaction molecules (STIMs), respectively. This report provides an overview of the (patho) physiological importance of SOCE in blood cells implicated in thrombosis and thrombo-inflammation, i.e. platelets and immune cells. We also discuss the physiological consequences of dysregulated SOCE in platelets and immune cells and the potential of SOCE inhibition as a therapeutic option to prevent or treat arterial thrombosis as well as thrombo-inflammatory disease states such as ischemic stroke.

Original languageEnglish
Pages (from-to)39-48
Number of pages10
JournalCell Calcium
Volume77
DOIs
Publication statusPublished - Jan 2019

Keywords

  • SOCE
  • Platelets
  • Immune cells
  • Arterial thrombosis
  • Ischemic stroke
  • Thrombo-inflammation
  • REGULATORY T-CELLS
  • CA2+ ENTRY
  • ARTERIAL THROMBOSIS
  • HUMAN PLATELETS
  • CRAC CHANNEL
  • ISCHEMIC-STROKE
  • TRP CHANNELS
  • NEUTROPHIL RECRUITMENT
  • EFFECTOR FUNCTIONS
  • GLYCOPROTEIN VI

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