ArticleHistochemistry and cell biology2026
Histochemical characterization of muscularis macrophage loss and disruption of a miR-93-5p-AHNAK neuro-immune axis in Hirschsprung's disease.
Article in Histochemistry and cell biology, 2026. 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.
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Who cites it
1 citing paper in PubMed.
- Macrophage-enteric nervous system crosstalk in Hirschsprung disease and associated enterocolitis: a focused narrative review with clinical implications.Pediatric surgery international · 2026Review
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Authors and funding
7 authors.
Funding
Abstract
Hirschsprung's disease (HSCR) is a congenital disorder of the distal intestine characterized by aganglionosis of the enteric nervous system. While defective migration of neural crest-derived precursors is a well-established hallmark, how the intestinal microenvironment contributes to impaired neuronal support remains poorly understood. Here, we combined histochemical analyses of human HSCR colon with functional assays to investigate the role of muscularis macrophages (MMs) and a miR-93-5p-AHNAK pathway in regulating enteric neurons. Using immunohistochemistry and immunofluorescence on ganglionic and aganglionic segments, we mapped the density, spatial distribution, and phenotype of MMs, and quantified the expression of miR-93-5p and its predicted target AHNAK. In vitro, polarized M2-like macrophages were cocultured with enteric neuronal cell lines to assess neuronal migration, proliferation, and apoptosis. Gain-of-function and loss-of-function approaches for miR-93-5p, together with a dual-luciferase reporter assay, were used to validate AHNAK as a direct target. M2-like MMs (CD163
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Registered trials
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