Evidence map›Paper›PMID 38233402›Full record

ArticleScientific reports2024

A computational model of stem cells' internal mechanism to recapitulate spatial patterning and maintain the self-organized pattern in the homeostasis state.

Najme Khorasani, Mehdi Sadeghi

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
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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

2 authors.

Najme KhorasaniSchool of Biological Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran. najme.khorasani@ipm.ir.
Mehdi SadeghiNational Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complex functioning of multi-cellular tissue development relies on proper cell production rates to replace dead or differentiated specialized cells. Stem cells are critical for tissue development and maintenance, as they produce specialized cells to meet the tissues' demands. In this study, we propose a computational model to investigate the stem cell's mechanism, which generates the appropriate proportion of specialized cells, and distributes them to their correct position to form and maintain the organized structure in the population through intercellular reactions. Our computational model focuses on early development, where the populations overall behavior is determined by stem cells and signaling molecules. The model does not include complicated factors such as movement of specialized cells or outside signaling sources. The results indicate that in our model, the stem cells can organize the population into a desired spatial pattern, which demonstrates their ability to self-organize as long as the corresponding leading signal is present. We also investigate the impact of stochasticity, which provides desired non-genetic diversity; however, it can also break the proper boundaries of the desired spatial pattern. We further examine the role of the death rate in maintaining the system's steady state. Overall, our study sheds light on the strategies employed by stem cells to organize specialized cells and maintain proper functionality. Our findings provide insight into the complex mechanisms involved in tissue development and maintenance, which could lead to new approaches in regenerative medicine and tissue engineering.

Indexed as

Stem CellsTissue EngineeringCell DifferentiationHomeostasisRegenerative Medicine

Identifiers

PMID38233402
PMCPMC10794714

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Registered trials

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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 OpenQuestion graph.