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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

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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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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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Necrosis01:16

Necrosis

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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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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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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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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Related Experiment Video

Updated: Jun 28, 2025

Author Spotlight: THP-1 Macrophage Response to LPS/ATP &#8212; Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
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Nanomaterials-induced programmed cell death: Focus on mitochondria.

Shijia Qiao1, Yiyuan Kang1, Xiner Tan1

  • 1Stomatological Hospital, Southern Medical University, Guangzhou 510280, China.

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Summary

Nanomaterials can cause cell death through programmed pathways like apoptosis. This review focuses on mitochondria

Keywords:
ApoptosisMitochondriaNanomaterialsProgrammed cell death

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Area of Science:

  • Biomedical Science
  • Materials Science
  • Toxicology

Background:

  • Nanomaterials are increasingly used in various fields, including biomedical applications.
  • Their interaction with biological systems can lead to unintended cellular damage and death.
  • Programmed cell death, including apoptosis, ferroptosis, necroptosis, and pyroptosis, is a primary outcome of nanotoxicity.

Purpose of the Study:

  • To review the molecular mechanisms of nanomaterial-induced programmed cell death.
  • To highlight the critical role of mitochondria in these processes.
  • To identify potential therapeutic targets for mitigating nanotoxicity.

Main Methods:

  • Literature review of existing studies on nanomaterial-induced cell death.
  • Focus on research detailing mitochondrial involvement in programmed cell death pathways.
  • Analysis of signaling pathways initiated or transmitted by mitochondria.

Main Results:

  • Mitochondria play a central role in initiating and mediating nanomaterial-induced programmed cell death.
  • Specific molecular pathways involving mitochondria are crucial for different types of programmed cell death.
  • Understanding these mitochondrial mechanisms is key to addressing nanotoxicity.

Conclusions:

  • Mitochondria are pivotal in nanomaterial-induced programmed cell death.
  • Targeting mitochondrial pathways offers potential strategies for preventing and treating nanotoxicity.
  • Further research into these mechanisms is essential for safe nanomaterial application.