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Overview of Cell Death01:30

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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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The Extrinsic Apoptotic Pathway01:17

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Autophagic Cell Death01:18

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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.
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Apoptosis01:30

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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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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Necrosis01:16

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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”.
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In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila
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Cracking the Cell Death Code.

Carla V Rothlin1,2, Sourav Ghosh2,3

  • 1Department of Immunobiology, School of Medicine, Yale University, New Haven, Connecticut 06520, USA.

Cold Spring Harbor Perspectives in Biology
|September 25, 2019
PubMed
Summary
This summary is machine-generated.

Cell death, whether programmed or accidental, triggers specific cellular responses. A new "cell death code" integrates intrinsic, environmental, and responder signals to guide tissue remodeling, renewal, and repair.

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Tissue Homeostasis

Background:

  • Cell death is a continuous process throughout life, essential for development, homeostasis, and repair.
  • Different types of cell death (scheduled, homeostasis, accidental) elicit distinct responses from surrounding cells.
  • Understanding these responses is crucial for tissue sculpting, cell replenishment, and damage repair.

Purpose of the Study:

  • To propose a framework for understanding cell death responses.
  • To integrate various signals that initiate effector responses after cell death.
  • To introduce a threefold "cell death code" for cell death signaling.

Main Methods:

  • Conceptual framework development.
  • Integration of existing knowledge on cell death and tissue response.
  • Proposal of a novel signaling model.

Main Results:

  • Cell death initiates specific effector cascades based on its context.
  • A unified "cell death code" is proposed, integrating multiple information sources.
  • This code governs tissue remodeling, renewal, and repair processes.

Conclusions:

  • Cell death signaling is complex, involving intrinsic, environmental, and responder factors.
  • The proposed "cell death code" offers a new perspective on regulating tissue dynamics.
  • This framework can advance research in developmental biology, regenerative medicine, and pathology.