Circadian disruption and ROS-NLRP3 signaling mediate sleep deprivation-enhanced silica nanoparticle toxicity in lacrimal glands.

Sleep deprivation (SD) and exposure to engineered nanomaterials such as silica nanoparticles (SiNPs) are emerging risk factors for ocular surface disorders, particularly dry eye disease. However, the molecular mechanisms underlying their combined impact on lacrimal gland function remain unclear. In this study, we investigated the synergistic effects of SD and SiNPs exposure on circadian regulation, oxidative stress, inflammation, and structural integrity of the extraorbital lacrimal glands (ELGs) in C57BL/6J mice.

Plin2 Coordinates Immune and Metabolic Reprogramming in Lacrimal Gland Aging.

Purpose: Aging impairs lacrimal gland function, contributing to dry eye syndrome and reduced quality of life. This study aimed to identify core molecular regulators of lacrimal gland aging and delineate their roles in immune imbalance and metabolic dysfunction.

Methods: Bulk transcriptomic profiling and single-cell RNA sequencing (scRNA-seq) were performed on lacrimal glands from young and aged C57BL/6 mice.

Chronic Jet Lag Disrupts Circadian Rhythms and Induces Hyperproliferation in Murine Lacrimal Glands via ROS Accumulation.

Purpose: Chronic jet lag (CJL) is known to disrupt circadian rhythms, which regulate various physiological processes, including ocular surface homeostasis. However, the specific effects of CJL on lacrimal gland function and the underlying cellular mechanisms remain poorly understood.

Methods: A CJL model was established using C57BL/6J mice.

Leptin Receptor Deficiency-Associated Diabetes Disrupts Lacrimal Gland Circadian Rhythms and Contributes to Dry Eye Syndrome.

Purpose: This study investigated the impact of hyperglycemia in type 2 diabetes mellitus (T2DM) on the circadian rhythms and function of lacrimal glands (LGs) in contributing to dry eye syndrome. We assessed the effects of hyperglycemia on circadian gene expression, immune cell recruitment, neural activity, and metabolic pathways, and evaluated the effectiveness of insulin in restoring normal LG function.

Methods: Using a T2DM mouse model (db/db mice), circadian transcriptomic changes in LGs were analyzed through RNA sequencing over a 24-hour period.

Long-term high fructose intake reprograms the circadian transcriptome and disrupts homeostasis in mouse extra-orbital lacrimal glands.

This study aims to explore the effects of long-term high fructose intake (LHFI) on the structure, functionality, and physiological homeostasis of mouse extra-orbital lacrimal glands (ELGs), a critical component of ocular health. Our findings reveal significant reprogramming of the circadian transcriptome in ELGs following LHFI, alongside the activation of specific inflammatory pathways, as well as metabolic and neural pathways. Notably, LHFI resulted in increased inflammatory infiltration, enhanced lipid deposition, and reduced nerve fiber density in ELGs compared to controls.

Chronic sleep deprivation impairs retinal circadian transcriptome and visual function.

Sleep loss is common in modern society and is increasingly associated with eye diseases. However, the precise effects of sleep loss on retinal structure and function, particularly on the retinal circadian system, remain largely unexplored. This study investigates these effects using a chronic sleep deprivation (CSD) model in mice.