Lacrimal Secretory Niche Remodeling in Dry Eye Disease: Single-Cell and Spatial Insights into Acinar Dysfunction.
- 1Faculty of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha 410208, China.
- 2Institute of Ophthalmology and Otolaryngology of Chinese Medicine, Changsha 410208, China.
Abstract
Reduced tear output can arise from altered neural regulation, impaired epithelial secretion, or loss of secretory tissue, with different implications for recovery. This focused narrative review integrates physiological, single-cell, spatial, organoid, and mechanistic studies identified through a structured PubMed search and targeted reference checking. We examine how remodeling of the lacrimal secretory niche affects acinar secretory competence, the capacity of viable acinar cells to convert stimulation into coordinated fluid, electrolyte, and protein secretion. Omics studies identify disease-associated expression patterns and candidate interactions, while selected perturbation studies link neural, inflammatory, and metabolic mechanisms to secretory dysfunction. We use residual functional reserve as a working concept for secretion that surviving tissue and its supporting niche can recruit through stimulation or relief of suppression. Potentially reversible functional suppression, persistent niche dysfunction, and structural failure describe overlapping constraints on secretion, not validated disease stages. These descriptions are distinct from the cellular, glandular, and lacrimal functional-unit levels at which outcomes are measured. The framework organizes questions about mechanism and recovery but does not establish a clinical treatment algorithm. Progress requires functional testing of candidate mechanisms and assessment of recovery at the level relevant to each claim.
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BibTeX
@article{zhong2026lacrimal,
title = {{Lacrimal Secretory Niche Remodeling in Dry Eye Disease: Single-Cell and Spatial Insights into Acinar Dysfunction.}},
author = {Yuan Zhong and Xiyuan Liu and Qinghua Peng and Jun Peng},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15191828},
url = {https://europepmc.org/article/MED/42882526},
note = {CC BY},
}
RIS
TY - JOUR
TI - Lacrimal Secretory Niche Remodeling in Dry Eye Disease: Single-Cell and Spatial Insights into Acinar Dysfunction.
AU - Yuan Zhong
AU - Xiyuan Liu
AU - Qinghua Peng
AU - Jun Peng
PY - 2026
DA - 2026/10/08
JO - Cells
DO - 10.3390/cells15191828
UR - https://europepmc.org/article/MED/42882526
AB - Reduced tear output can arise from altered neural regulation, impaired epithelial secretion, or loss of secretory tissue, with different implications for recovery. This focused narrative review integrates physiological, single-cell, spatial, organoid, and mechanistic studies identified through a structured PubMed search and targeted reference checking. We examine how remodeling of the lacrimal secretory niche affects acinar secretory competence, the capacity of viable acinar cells to convert stimulation into coordinated fluid, electrolyte, and protein secretion. Omics studies identify disease-associated expression patterns and candidate interactions, while selected perturbation studies link neural, inflammatory, and metabolic mechanisms to secretory dysfunction. We use residual functional reserve as a working concept for secretion that surviving tissue and its supporting niche can recruit through stimulation or relief of suppression. Potentially reversible functional suppression, persistent niche dysfunction, and structural failure describe overlapping constraints on secretion, not validated disease stages. These descriptions are distinct from the cellular, glandular, and lacrimal functional-unit levels at which outcomes are measured. The framework organizes questions about mechanism and recovery but does not establish a clinical treatment algorithm. Progress requires functional testing of candidate mechanisms and assessment of recovery at the level relevant to each claim.
SN - 2073-4409
ER -