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Apoptosis

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.

The Intrinsic Apoptotic Pathway

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...

Caspases

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.

Autophagic Cell Death

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...

Overview of Cell Death

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 Autophagy

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...

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Related Experiment Video

Updated: Jul 6, 2026

The Creation of a Rat Model for Osteosarcopenia via Ovariectomy

The Creation of a Rat Model for Osteosarcopenia via Ovariectomy

Published on: February 21, 2025

Nuclear apoptosis contributes to sarcopenia.

Stephen E Alway¹, Parco M Siu

¹Laboratory of Muscle Biology and Sarcopenia, Division of Exercise Physiology, West Virginia University School of Medicine, Morgantown, WV 26506-9227, USA. salway@hsc.wvu.edu

Exercise and Sport Sciences Reviews

|March 26, 2008

Summary

Multinucleated cells, like muscle fibers, can lose nuclei through apoptosis without cell death, potentially causing muscle atrophy and sarcopenia. Chronic activity may reduce this nuclear apoptosis, mitigating sarcopenia.

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Area of Science:

Cell Biology
Muscle Physiology
Aging Research

Background:

Apoptosis typically leads to the destruction of single-nucleated cells via DNA fragmentation.
Multinucleated cells, such as muscle fibers, present a unique case where apoptosis might affect individual nuclei without causing complete cell death.

Purpose of the Study:

To investigate the phenomenon of nuclear apoptosis in multinucleated muscle fibers.
To explore the link between nuclear loss and the development of muscle atrophy and sarcopenia.
To determine if chronic physical activity influences apoptotic signaling in muscle fibers and impacts sarcopenia.

Main Methods:

The study likely involved examining muscle tissue samples to identify signs of apoptosis within individual nuclei.
Methods may include molecular biology techniques to assess apoptotic markers and nuclear integrity.
Comparative analysis between different activity levels (e.g., sedentary vs. chronically active) would be employed.

Main Results:

Evidence suggests that multinucleated muscle fibers can undergo apoptosis of single nuclei (nuclear apoptosis).
This selective loss of nuclei is hypothesized to contribute significantly to muscle atrophy and the aging-related condition, sarcopenia.
Increased chronic physical activity appears to attenuate apoptotic signaling pathways, potentially offering a protective effect against sarcopenia.

Conclusions:

Nuclear apoptosis is a plausible mechanism contributing to sarcopenia in multinucleated cells like muscle fibers.
Targeting or modulating apoptotic signaling in muscle nuclei could be a therapeutic strategy for combating age-related muscle loss.
Chronic activity's role in reducing sarcopenia warrants further investigation into its molecular mechanisms.