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Related Concept Videos

Autophagic Cell Death01:18

Autophagic Cell Death

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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.
Autophagy and Apoptosis
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Phagocytosis of Apoptotic Cells01:17

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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. 
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Autophagy01:27

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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The Intrinsic Apoptotic Pathway01:31

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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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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 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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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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The cellular autophagy/apoptosis checkpoint during inflammation.

Jeannette S Messer1

  • 1Department of Medicine, Knapp Center for Biomedical Discovery, University of Chicago, 900 E. 57th Street, 9th Floor, Chicago, IL, 60637, USA. jmesser@medicine.bsd.uchicago.edu.

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Cell death in inflammatory diseases hinges on the balance between autophagy and apoptosis. Targeting the autophagy/apoptosis checkpoint offers a novel therapeutic strategy for managing inflammatory conditions.

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Area of Science:

  • Cell Biology
  • Immunology
  • Pathology

Background:

  • Cell death significantly influences inflammatory disease severity.
  • The balance between pro-survival autophagy and pro-death apoptosis determines cell fate during inflammation.
  • Autophagy and apoptosis are interconnected processes with a critical checkpoint for cell fate commitment.

Purpose of the Study:

  • To review the concept and significance of the autophagy/apoptosis checkpoint in inflammation.
  • To elucidate the inflammatory mechanisms leading to this checkpoint.
  • To discuss the regulatory mechanisms governing the autophagy/apoptosis checkpoint.

Main Methods:

  • Literature review of autophagy and apoptosis pathways in inflammation.
  • Analysis of molecular mechanisms regulating cell death decisions.
  • Synthesis of current understanding of the autophagy/apoptosis checkpoint.

Main Results:

  • Inflammation involves a critical checkpoint where cells commit to either autophagy or apoptosis.
  • Understanding this checkpoint is key to comprehending inflammatory disease progression.
  • Dysregulation of this balance contributes to various inflammatory pathologies.

Conclusions:

  • The autophagy/apoptosis checkpoint is a crucial determinant of inflammatory disease outcomes.
  • Targeting this checkpoint presents a novel therapeutic avenue for inflammatory diseases.
  • Further research into checkpoint regulation can lead to innovative treatments for conditions involving aberrant cell death.