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Eryptosis: Ally or Enemy.

Marilena Briglia1, Maria Antonia Rossi1, Caterina Faggio2

  • 1Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno d`Alcontres, 31, 98166 S.Agata-Messina, Italy.

Current Medicinal Chemistry
|November 19, 2016
PubMed
Summary

Eryptosis, or suicidal erythrocyte death, removes damaged red blood cells but excessive cell death can cause anemia. This process is crucial for removing infected cells, like in malaria, without pathogen resistance.

Keywords:
Eryptosisanaemiabeta-thalassemiacytosolic Ca2+diabetes.malaria

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Area of Science:

  • Cell Biology
  • Hematology
  • Pathophysiology

Background:

  • Erythrocytes can undergo injury prior to senescence, leading to suicidal erythrocyte death (eryptosis).
  • Eryptosis involves cell shrinkage, membrane blebbing, and phosphatidylserine exposure, marking cells for macrophage engulfment.
  • Triggers include oxidative stress, increased cytosolic calcium, and p38 kinase activation.

Purpose of the Study:

  • To explore the mechanism and implications of eryptosis.
  • To investigate the role of eryptosis in various clinical conditions and disease management.

Main Methods:

  • The study reviews mechanisms of eryptosis, including cellular changes and molecular triggers.
  • It examines conditions associated with enhanced eryptosis and its potential as a therapeutic target.

Main Results:

  • Enhanced eryptosis is observed in numerous conditions like diabetes, malaria, and sickle cell anemia.
  • Eryptosis aids in removing defective and infected erythrocytes, potentially reducing parasitemia.
  • Inducing eryptosis offers a strategy against malaria without pathogen resistance, but excessive eryptosis can lead to anemia.

Conclusions:

  • Eryptosis is a key removal mechanism for compromised erythrocytes, preventing hemolysis.
  • Targeting eryptosis may be beneficial in managing diseases like malaria.
  • Balancing eryptosis is crucial to avoid adverse effects like anemia and microcirculation compromise.