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Related Concept Videos

Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
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...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
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Lifecycle of Erythrocytes01:22

Lifecycle of Erythrocytes

Erythrocytes, also known as red blood cells, constantly move through blood capillaries. As a result, they damage their plasma membrane due to the continuous friction. Typically, after 100 to 120 days, erythrocytes become rigid and fragile as they wear out. As they pass through small vessels in the spleen and liver, they can get trapped and break apart into fragments.
The resident phagocytic macrophages deal with these damaged cells by engulfing them and separating their globin and heme groups.
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
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Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...

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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

Killing me softly - suicidal erythrocyte death.

Elisabeth Lang1, Syed M Qadri, Florian Lang

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

The International Journal of Biochemistry & Cell Biology
|May 8, 2012
PubMed
Summary

Eryptosis, or programmed red blood cell death, involves cell shrinkage and membrane changes, preventing hemolysis. It is triggered by various stressors and implicated in numerous diseases, potentially leading to anemia.

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Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
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Area of Science:

  • Hematology
  • Cell Biology
  • Physiology

Background:

  • Erythrocytes (red blood cells) can undergo programmed cell death, termed eryptosis.
  • Eryptosis is characterized by cell shrinkage, membrane blebbing, and phospholipid scrambling, preventing hemolysis.
  • This process is crucial for removing aged or damaged erythrocytes.

Purpose of the Study:

  • To explore the mechanisms and triggers of eryptosis.
  • To identify factors that modulate eryptosis.
  • To understand the clinical relevance of eryptosis in various diseases.

Main Methods:

  • Review of existing literature on eryptosis.
  • Analysis of signaling pathways involved in eryptosis, including calcium influx and ceramide signaling.
  • Examination of factors influencing eryptosis, such as oxidative stress, hyperosmolarity, and specific molecules.
  • Investigation of genetic and disease models exhibiting altered eryptosis.

Main Results:

  • Eryptosis is stimulated by increased intracellular calcium (Ca2+) and ceramide.
  • Diverse stimuli, including oxidative stress, hyperosmolarity, and numerous xenobiotics, can trigger eryptosis.
  • Nitric oxide and catecholamines can inhibit eryptosis, while erythropoietin has a complex role.
  • Accelerated eryptosis, if not balanced by erythropoiesis, can lead to anemia and impede microcirculation.

Conclusions:

  • Eryptosis is a regulated process with significant implications for red blood cell homeostasis.
  • Dysregulation of eryptosis is associated with various clinical conditions, including anemia and microcirculatory disturbances.
  • Further research into eryptosis modulation may offer therapeutic strategies for related diseases.