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Related Concept Videos

Autophagy01:27

Autophagy

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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.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
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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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Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
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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. 
Normal cells contain receptors that prevent them from being recognized...
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Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

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Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
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Related Experiment Video

Updated: Sep 6, 2025

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice
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In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

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Mitophagy and Neuroinflammation: A Compelling Interplay.

Nikolaos Charmpilas1, Evandro Fei Fang2,3,4, Konstantinos Palikaras5

  • 1Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Ageing-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.

Current Neuropharmacology
|June 28, 2022
PubMed
Summary

Impaired mitophagy, the process of degrading damaged mitochondria, contributes to neuroinflammation and neurodegenerative diseases. Enhancing mitophagy offers a potential therapeutic strategy for brain health.

Keywords:
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Area of Science:

  • Cellular Biology
  • Neuroscience
  • Pathology

Background:

  • Mitochondria are crucial for energy production but also generate metabolic stress.
  • Mitochondrial dysfunction is linked to various human diseases, particularly neurodegeneration.
  • Mitophagy selectively removes damaged mitochondria, maintaining cellular health.

Purpose of the Study:

  • To explore the relationship between mitophagy and neuroinflammation.
  • To highlight mitophagy as a therapeutic target for neurodegenerative disorders.

Main Methods:

  • Literature review on mitophagy and neuroinflammation.
  • Analysis of cellular mechanisms linking mitochondrial homeostasis and brain pathology.

Main Results:

  • Defective mitophagy leads to cellular senescence and sustained neuroinflammation.
  • This process can result in neuronal cell death and compromised brain homeostasis.
  • Mitophagy dysfunction is a key factor in neurodegenerative disease progression.

Conclusions:

  • Mitophagy plays a critical role in preventing neuroinflammation and neurodegeneration.
  • Targeting mitophagy presents a promising therapeutic avenue for treating neurodegenerative conditions.