Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Erythropoiesis01:14

Erythropoiesis

Red blood cells  (RBCs) transport oxygen to all body tissues. These cells survive only for 120 days and then need to be replenished. Erythropoiesis is the process of RBC production. In healthy individuals, erythropoiesis ensures all tissues are amply supplied with oxygen. In addition, blood loss due to injury leads to a drop in the physiological oxygen level that will cause erythropoiesis. Any defect in erythropoiesis leads to several physiological disorders, including thalassemia, anemia, and...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Intracellular cyclophilin A is an important Ca(2+) regulator in platelets and critically involved in arterial thrombus formation.

Blood·2012
Same author

Carbon monoxide-sensitive apoptotic death of erythrocytes.

Basic & clinical pharmacology & toxicology·2012
Same author

Induction of apoptotic erythrocyte death by rotenone.

Toxicology·2012
Same author

Regulation of Orai1/STIM1 by the kinases SGK1 and AMPK.

Cell calcium·2012
Same author

OSR1-sensitive regulation of Na+/H+ exchanger activity in dendritic cells.

American journal of physiology. Cell physiology·2012
Same author

Downregulation of ClC-2 by JAK2.

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology·2012
Same journal

ALKBH4 Promotes Osteogenesis via Epigenetic Regulation of BMP2-Wnt/β-Catenin Signaling in Cervical Spine OPLL.

IUBMB life·2026
Same journal

Single-Sequence Deep Learning Delivers Crystal-Quality Models of Covalent K-Ras G12 Hotspot Complexes.

IUBMB life·2026
Same journal

Mechanism of PCSK9-Mediated Macrophage Activation via the CAP1/NF-κB Pathway in CAWS-Induced Kawasaki Disease Vasculitis.

IUBMB life·2026
Same journal

Hormesis and the Golden Ratio: Toward a Universal Estimator of Adaptive Capacity.

IUBMB life·2026
Same journal

MicroRNAs in HPV-Associated Carcinogenesis: Potential Biomarkers in Oropharyngeal and Cervical Cancers.

IUBMB life·2026
Same journal

PGAM1 Orchestrates Cell Cycle Progression, Glycolytic Reprogramming, and Immunosuppressive Microenvironment in Triple-Negative Breast Cancer.

IUBMB life·2026
See all related articles

Related Experiment Video

Updated: Jul 2, 2026

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
09:15

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore

Published on: January 21, 2020

Erythrocyte programmed cell death.

Michael Föller1, Stephan M Huber, Florian Lang

  • 1Department of Physiology, University of Tübingen, Germany.

IUBMB Life
|August 23, 2008
PubMed
Summary
This summary is machine-generated.

Eryptosis, or programmed red blood cell death, involves cell shrinkage and phosphatidylserine exposure, leading to macrophage engulfment. Imbalances in eryptosis contribute to anemia, highlighting the need for regulated cell death.

More Related Videos

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells
12:44

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Published on: October 11, 2012

Related Experiment Videos

Last Updated: Jul 2, 2026

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
09:15

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore

Published on: January 21, 2020

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells
12:44

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Published on: October 11, 2012

Area of Science:

  • Cell Biology
  • Hematology
  • Physiology

Background:

  • Eryptosis, the suicidal death of erythrocytes, is a regulated process characterized by cell shrinkage, membrane blebbing, and phosphatidylserine exposure.
  • This process is recognized by macrophages, leading to the clearance of affected red blood cells.
  • Dysregulation of eryptosis is implicated in various diseases and can lead to anemia.

Purpose of the Study:

  • To elucidate the molecular mechanisms and triggers of eryptosis.
  • To identify factors that inhibit or promote eryptosis.
  • To understand the role of eryptosis in maintaining erythrocyte homeostasis and its contribution to anemia.

Main Methods:

  • Review and synthesis of existing literature on eryptosis triggers, signaling pathways, and associated diseases.
  • Analysis of the molecular players involved in eryptosis, including calcium ions (Ca2+), ceramide, and prostaglandin E2 (PGE2).
  • Examination of the balance between proeryptotic and antieryptotic mechanisms.

Main Results:

  • Numerous triggers for eryptosis have been identified, including osmotic shock, oxidative stress, and various chemical and biological agents.
  • Key signaling pathways involve Ca2+ influx and ceramide generation, leading to membrane scrambling and cell shrinkage.
  • Eryptosis can be inhibited by factors like erythropoietin and nitric oxide (NO).

Conclusions:

  • Eryptosis is a crucial mechanism for removing defective erythrocytes, preventing hemolysis.
  • However, excessive eryptosis can lead to anemia, underscoring the importance of a balanced regulation.
  • Maintaining the delicate balance between proeryptotic and antieryptotic pathways is essential for erythrocyte health.