ArticleCell death discovery2025
Acetylcholine muscarinic M2 receptor maintains human Schwann-like adipose-derived phenotype in the absence of differentiating medium.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Chemogenetic Schwann cell activation impairs early myelination and triggers adult demyelination in the peripheral nervous system.Frontiers in cellular neuroscience · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Human adipose-derived stem cells (ASCs), differentiated in vitro towards Schwann-like phenotype (hdASCs), have been suggested as an alternative source of Schwann cells (SCs). However, although they seem a good alternative, their differentiation is unstable, losing their SC-like phenotype following growth factor withdrawal. Rat and human SCs and rat dASCs have been characterized for acetylcholine M2 muscarinic receptor subtype that plays a strategic role in the regulation of their differentiation. Here, we evaluated the M2 muscarinic receptor activation in controlling hdASC proliferation and stabilization of the hdASC phenotype. In accordance with our data in rats, M2 stimulation results in a reversible decrease of cell growth and migration in hdASCs, negatively modulates proliferation markers and upregulates differentiation markers. Remarkably, hdASC differentiation can be stabilized by M2 receptor activation in the absence of differentiation media maintaining a spindle-shaped morphology and SC-like marker expression. These results show that the M2 receptor enhances the hdASC phenotype, maintaining the expression of key glial markers and supporting their pro-regenerative properties.
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Registered trials
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.