Evidence map›Paper›PMID 41004006›Full record

ReviewSub-cellular biochemistry2025

Macromolecular Crowding in Cell Stress and Death.

Michael A Model

Abstract readReview
PubMed Publisher
In one paragraph

Review in Sub-cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Michael A ModelDepartment of Biological Science, Kent State University, Kent, OH, USA. mmodel@kent.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To study macromolecular crowding (MC) in living cells, one needs a method to measure it. Several existing approaches to quantify MC address slightly different aspects of crowding. If we define MC through protein concentration, it can be measured by quantitative phase imaging coupled with volume determination; both can be realized on a standard bright-field microscope. Osmotic cell theory can help identify the essential factors that control MC. Nevertheless, there are still many gaps in our understanding of MC regulation and, in particular, of the interrelationship between MC and cell stress or damage. Experiments show that MC is subject to homeostatic control and returns to its resting values following various disturbances. Severe cell damage causes an accumulation of water and a decrease in MC; however, based on limited data, water accumulation is restricted to one area of the cell (necrotic bleb), while the rest of the cell remains at normal density. Similar heterogeneous water distribution is observed in vacuolated mammalian cells. Intermediate degrees of stress tend to produce dehydration and an increase in MC. Apoptotic shrinkage is one common example of stress-induced dehydration, but the effect may be more general. A hypothesis on its mechanism is proposed.

Indexed as

ApoptosisMacromolecular SubstancesStress, PhysiologicalAnimalsCell DeathHumansOsmotic PressureWaterMacromolecular SubstancesWaterApoptotic volume decreaseCell volumeDehydrationIntracellular waterMacromolecular crowdingNecrotic volume increaseQuantitative phase contrastTransmission-through-dye

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.