ArticleFrontiers in cell and developmental biology2020
A Reverse-Osmosis Model of Apoptotic Shrinkage.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
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- Macromolecular Crowding in Cell Stress and Death.Sub-cellular biochemistry · 2025Review
- A Response to Article "Selenium-Modified Chitosan Induces HepG2 Cell Apoptosis and Differential Protein Analysis" [Letter].Cancer management and research · 2023Article
- Article
- Growth and Drug Interaction Monitoring of NIH 3T3 Cells by Image Analysis and Capacitive Biosensor.Micromachines · 2021Article
- Early mechanical selection of cell extrusion and extrusion signaling in cancer.Current opinion in cell biology · 2021Review
- The Role of WAVE2 Signaling in Cancer.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The standard theory of apoptotic volume decrease (AVD) posits activation of potassium and/or chloride channels, causing an efflux of ions and osmotic loss of water. However, in view of the multitude of possible channels that are known to support apoptosis, a model based on specific signaling to a channel presents certain problems. We propose another mechanism of apoptotic dehydration based on cytoskeletal compression. As is well known, cytoskeleton is not strong enough to expel a substantial amount of water against an osmotic gradient. It is possible, however, that an increase in intracellular pressure may cause an initial small efflux of water, and that will create a small concentration gradient of ions, favoring their exit. If the channels are open, some ions will exit the cell, relieving the osmotic gradient; in this way, the process will be able to continue. Calculations confirm the possibility of such a mechanism. An increase in membrane permeability for water or ions may also result in dehydration if accompanied even by a constant cytoskeletal pressure. We review the molecular processes that may lead to apoptotic dehydration in the context of this model.
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