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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...
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Cellular Injury V: Apoptosis and Autophagy01:22

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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...
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Overview of Regeneration and Repair01:19

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Regeneration and repair processes are critical in healing damages caused by injury, disease, and aging. In regeneration, the damaged tissue is entirely replaced with new growth that restores the original architecture and function. In contrast, tissue repair usually results in a fixed tissue architecture involving scar formation. Scars generally do not reestablish tissue function and may also exhibit structural abnormalities at the injury site.
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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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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...
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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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Cell death: a program to regenerate.

Sophie Vriz1, Silke Reiter2, Brigitte Galliot2

  • 1Collège de France, Center for Interdisciplinary Research in Biology (CIRB), Paris, France; University Paris-Diderot, Paris, France.

Current Topics in Developmental Biology
|February 12, 2014
PubMed
Summary
This summary is machine-generated.

Cell death triggers regeneration in adult animals by releasing instructive signals and eliminating suppressor cells. This "regenerative cell death" involves reactive oxygen species (ROS) and caspase-dependent signaling pathways.

Keywords:
ApoptosisApoptotic bodiesMAPKProstaglandinROSWnt

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Regenerative Medicine

Background:

  • Cell death is increasingly recognized as a crucial initiator of regeneration in various adult animal models, including Drosophila, Hydra, planarians, zebrafish, and mice.
  • Injury-induced cell death can trigger regeneration through immediate instructive signaling or sustained derepression of regenerative pathways by eliminating suppressor cells.
  • The concept of
  • regenerative cell death
  • suggests common underlying mechanisms, but these are not yet fully understood.

Purpose of the Study:

  • To review the key parameters of regenerative cell death, including injury-induced proapoptotic signals, signals released by dying cells, cellular responses, and their temporal dynamics.
  • To explore common signaling molecules and pathways involved in initiating regeneration following cell death.
  • To elucidate the complex paracrine signaling networks that orchestrate regenerative responses.

Main Methods:

  • Review of existing literature on cell death and regeneration across multiple model organisms.
  • Analysis of signaling molecules (e.g., ROS, cytokines, growth factors, prostaglandins, ATP) and pathways (e.g., MAPK, JNK, caspase-dependent) involved in regenerative cell death.
  • Examination of the temporal patterns of cell death and signaling during regeneration.

Main Results:

  • Reactive oxygen species (ROS) emerge as a common signal that triggers cell death via MAPK and/or JNK pathway activation, with varying production modes (brief pulse vs. repeated waves).
  • Regenerative cell death can be immediate (Hydra, Drosophila) or biphasic with delayed components (planarians, zebrafish).
  • Dying cells release diverse signaling molecules, including cytokines, growth factors, prostaglandins, and ATP, in a caspase-dependent manner, often involving ROS-producing cells that resist death to signal paracrinely.

Conclusions:

  • Regenerative cell death is a conserved phenomenon initiated by specific signaling events following injury.
  • ROS and caspase-dependent signaling pathways play critical roles in mediating regenerative cell death and subsequent tissue repair.
  • A complex paracrine signaling network involving ROS-producing, ROS-sensing, and effector cells orchestrates the initiation of regeneration.