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

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Apoptosis01:30

Apoptosis

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 reduction of the tissue.
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
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

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Related Experiment Video

Updated: Jun 19, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

[Programmed cell death as a target to interrupt the aging program].

F F Severin, V P Skulachev

    Advances in Gerontology = Uspekhi Gerontologii
    |October 16, 2009
    PubMed
    Summary
    This summary is machine-generated.

    Aging may be a genetically programmed process, not random damage. Inhibiting programmed cell death (apoptosis) via mitochondrial interventions offers a potential strategy to slow aging and maintain cellularity.

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    Induction and Validation of Cellular Senescence in Primary Human Cells
    08:18

    Induction and Validation of Cellular Senescence in Primary Human Cells

    Published on: June 20, 2018

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    Last Updated: Jun 19, 2026

    Techniques to Induce and Quantify Cellular Senescence
    06:51

    Techniques to Induce and Quantify Cellular Senescence

    Published on: May 1, 2017

    Induction and Validation of Cellular Senescence in Primary Human Cells
    08:18

    Induction and Validation of Cellular Senescence in Primary Human Cells

    Published on: June 20, 2018

    Area of Science:

    • Gerontology
    • Molecular Biology
    • Cellular Biology

    Background:

    • Aging research features two main theories: stochastic damage accumulation versus a genetically programmed process.
    • Recent evidence supports aging as a programmed final stage of development (ontogenesis).
    • This programmed aging concept predicts the existence of non-aging species and experimental interruption possibilities.

    Purpose of the Study:

    • To review evidence supporting the programmed aging theory.
    • To explore the role of apoptosis and mitochondrial reactive oxygen species (ROS) in aging.
    • To consider pharmacological interventions targeting the aging program.

    Main Methods:

    • Summarizing existing observations consistent with programmed aging predictions.
    • Analyzing the link between apoptosis, mitochondrial ROS, and cellularity decline.
    • Evaluating the use of mitochondria-targeted antioxidants and uncouplers as potential inhibitors.

    Main Results:

    • Observations align with predictions: non-aging species exist, and aging can be interrupted.
    • Interruption of the aging program involves inhibiting apoptosis mediated by mitochondrial ROS.
    • A key difference between young and old organisms is cellularity (functional cell number), which decreases due to apoptosis dominating proliferation.

    Conclusions:

    • Apoptosis, driven by mitochondrial ROS, appears to be the basis of the aging program.
    • Pharmacological strategies using mitochondria-targeted antioxidants and uncouplers can potentially inhibit the aging program.
    • These interventions mitigate age-related mitochondrial oxidative stress, thereby reducing apoptosis and preserving cellularity.