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Related Concept Videos

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
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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Necrosis01:16

Necrosis

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

Cellular Injury V: Apoptosis and Autophagy

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Related Experiment Video

Updated: May 24, 2026

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome
07:56

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

Lysosomal-mitochondrial cross-talk during cell death.

Urška Repnik1, Boris Turk

  • 1Department of Biochemistry and Molecular and Structural Biology, Jozef Stefan Institute, Jamova 39, SI-1000 Ljubljana, Slovenia. urska.repnik@ijs.si

Mitochondrion
|August 11, 2010
PubMed
Summary

Lysosomes initiate apoptosis by releasing enzymes that destabilize mitochondria, leading to cell death. This study explores the critical cross-talk between lysosomes and mitochondria in regulating cell fate.

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Last Updated: May 24, 2026

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome
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Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis
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Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

Published on: November 14, 2025

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Lysosomes are key degradative organelles involved in endocytosis, phagocytosis, and autophagy.
  • Lysosomal membrane destabilization triggers apoptosis, involving mitochondria.
  • Lysosomal proteases, like cathepsins, link lysosomes to mitochondrial pathways.

Purpose of the Study:

  • To discuss the intricate cross-talk between lysosomes and mitochondria during apoptosis.
  • To elucidate the molecular mechanisms linking lysosomal events to mitochondrial destabilization and cell death.
  • To explore the consequences of this lysosome-mitochondria crosstalk on cellular fate.

Main Methods:

  • Literature review and synthesis of existing research on lysosome-mitochondria interactions in apoptosis.
  • Analysis of molecular pathways involving lysosomal hydrolases (cathepsins) and their targets (BID, BCL-2).
  • Discussion of evidence linking lysosomal destabilization to mitochondrial outer membrane permeabilization and caspase activation.

Main Results:

  • Lysosomal destabilization leads to the release of cathepsins, which cleave BID and degrade BCL-2.
  • These events facilitate mitochondrial outer membrane permeabilization and cytochrome c release.
  • Lysosomes play a significant role in both intrinsic and potentially extrinsic apoptotic pathways.

Conclusions:

  • The cross-talk between lysosomes and mitochondria is a critical determinant of apoptosis.
  • Lysosomal integrity is crucial for preventing unwanted cell death.
  • Targeting lysosome-mitochondria interactions may offer therapeutic strategies for diseases involving aberrant apoptosis.