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  • Sleep Apnea affects...

Sleep Apnea affects lacrimal gland structure and function and induces dry eye

Medha BaranwalWritten by Medha Baranwal Published On 2022-06-19T20:00:06+05:30  |  Updated On 20 Jun 2022 10:00 AM GMT
Sleep Apnea affects lacrimal gland structure and function and induces dry eye
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China: Obstructive sleep apnea (OSA) disturbs the Hifα/Pparα/NF-κB signaling axis compromising lacrimal gland structure and function resulting in dry eye, finds a recent study in Investigative Ophthalmology & Visual Science. The findings imply that a therapeutic approach targeting the Hifα/Pparα/NF-κB pathway may be helpful in preserving the function of the lacrimal gland...

China: Obstructive sleep apnea (OSA) disturbs the Hifα/Pparα/NF-κB signaling axis compromising lacrimal gland structure and function resulting in dry eye, finds a recent study in Investigative Ophthalmology & Visual Science. The findings imply that a therapeutic approach targeting the Hifα/Pparα/NF-κB pathway may be helpful in preserving the function of the lacrimal gland and reducing dry eye symptoms exacerbated by OSA. 

Shaopan Wang, Xiamen University, Xiamen, Fujian, China, and colleagues conducted the study with the objective to determine the effect of obstructive sleep apnea syndrome (OSA) on lacrimal gland function and its mechanism. 

For this purpose, male mice aged seven to eight weeks were housed in cages with cyclic intermittent hypoxia to mimic OSA, and the control group was kept in a normal environment. Cornea changes were assessed using slit-lamp observation, fluorescein staining, and corneal sensitivity detection.

Phenol red cotton thread detected tear secretion, and the pathological changes of the lacrimal gland were observed by hematoxylin and eosin staining, oil red O staining, cholesterol and triglyceride kits, immunofluorescence staining, immunohistochemical staining, real-time polymerase chain reaction, transmission electron microscopy, and Western blot. 

The findings of the study were as follows:

· Studies revealed a decreased tear secretion, corneal epithelial defects, and corneal hypersensitivity.

· Myoepithelial cell damage, abnormal lipid accumulation, reduced cell proliferation, increased apoptosis, and inflammatory cell infiltration in the lacrimal gland were also seen.

· Hifα and NF-κB signaling pathways, moreover, were activated, while Pparα was downregulated, in the lacrimal glands of OSA mice.

· Fenofibrate treatment significantly alleviated pathological changes of the lacrimal gland induced by OSA.

"Our study for the first time confirmed a causative relationship between OSA and lacrimal gland dysfunction and pointed out a potential clinical treatment for OSA-related dry eye," the authors wrote in their study. 

"Our study suggests that OSA is a causative factor for dry eye disease and reveals a mechanism by which OSA could lead to abnormal lacrimal gland lipid metabolism through the Hif-Pparα signaling pathway, ultimately triggering manifestations of dry eye."

Reference:

Shaopan Wang, Xin He, Qingmin Li, Yuhan Zhang, Jiaoyue Hu, Rongrong Zong, Jingyi Zhuang, Andrew J. Quantock, Yingying Gao, Wei Li, Zuguo Liu; Obstructive Sleep Apnea Affects Lacrimal Gland Function. Invest. Ophthalmol. Vis. Sci. 2022;63(3):3. doi: https://doi.org/10.1167/iovs.63.3.3.

Obstructive Sleep ApneaInvestigative Ophthalmology & Visual Sciencedry eye
Source : Investigative Ophthalmology & Visual Science
Medha Baranwal
Medha Baranwal

    MSc. Biotechnology

    Medha Baranwal joined Medical Dialogues as an Editor in 2018 for Speciality Medical Dialogues. She covers several medical specialties including Cardiac Sciences, Dentistry, Diabetes and Endo, Diagnostics, ENT, Gastroenterology, Neurosciences, and Radiology. She has completed her Bachelors in Biomedical Sciences from DU and then pursued Masters in Biotechnology from Amity University. She has a working experience of 5 years in the field of medical research writing, scientific writing, content writing, and content management. She can be contacted at  editorial@medicaldialogues.in. Contact no. 011-43720751

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