Hyperlipidemia induces meibomian gland dysfunction

Bu, Jinghua; Wu, Yang; Cai, Xiaoxin; Jiang, Nan; Jeyalatha, M. Vimalin; Yu, Jingwen; He, Xin; He, Hui; Guo, Yanjie; Zhang, Mingjie; Quantock, Andrew J.; Liu, Zuguo; Li, Wei

doi:10.1016/j.jtos.2019.06.002

Cited by 57 publications

(45 citation statements)

References 52 publications

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“…The pathophysiological and molecular mechanisms between MGD and dyslipidemia have not been fully understood. The study by Bu et al 50 found that ApoE knockout mice that were a hypercholesterolemia animal model showed meibomian gland obstruction with meibomian gland atrophy. The ApoE knockout mice also showed increased inflammatory cell infiltration, abnormal meibomian gland acinar cell proliferation, and excessive keratinization in the meibomian gland.…”

Section: Discussionmentioning

confidence: 99%

“…The ApoE knockout mice also showed increased inflammatory cell infiltration, abnormal meibomian gland acinar cell proliferation, and excessive keratinization in the meibomian gland. 50 However, there is no molecular biology study to research the pathophysiological and molecular mechanisms in older patients. In this study, our subjects had an average age of 72.46 ± 10.30 years, which is the age in which the MG tends to atrophy.…”

Section: Discussionmentioning

confidence: 99%

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Characterization of Meibomian Gland Atrophy and the Potential Risk Factors for Middle Aged to Elderly Patients With Cataracts

Lin

Chen

et al. 2020

Trans. Vis. Sci. Tech.

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To explore the characteristics of meibomian gland (MG) atrophy and its potential risk factors in the age-related cataract population. Methods: Patients who underwent cataract surgery at age 40 or older were enrolled in this study. Preoperative clinical measurement records were obtained, including lipid layer thickness, tear meniscus height, noninvasive breakup time, and meiboscore. The meibomian gland atrophy ratio (MGAR) was measured by the ImageJ software. Univariate regression analysis and multivariate regression analysis were used to analyze the risk factors for MG atrophy. Results: Female patients had less atrophy of the MG compared with male patients. The MGAR, meiboscore, tear meniscus height (TMH), and lipid layer thickness (LLT) gradually increased with age. However, the noninvasive breakup time decreased with age. The multivariate regression analysis indicated that dyslipidemia and increased triglyceride levels were identified as independent protective factors for MG atrophy. We further stratified the model by sex, and the following results showed only in the female patients with dyslipidemia and increased triglyceride had decreased MG atrophy. No significant correlation was observed between MG atrophy and tear film parameters including TMH, noninvasive breakup time, and LLT. Conclusions: Our study suggests that age, sex, and diabetes are potential risk factors for MG atrophy. In addition, dyslipidemia and increased triglyceride levels are independent protective factors for MG atrophy in the elderly female population. Translational Relevance: MG atrophy is the leading cause of meibomian gland dysfunction. To study the characteristics and risk factors of MG atrophy in cataract patients would be helpful to predict and prevent postoperative development of MGD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Characterization of Meibomian Gland Atrophy and the Potential Risk Factors for Middle Aged to Elderly Patients With Cataracts

Lin

Chen

et al. 2020

Trans. Vis. Sci. Tech.

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“…In recent years, several clinical studies have demonstrated that moderate-to-severe MGD was associated with high total cholesterol and low-density lipoprotein blood levels [85,86]. Thereafter, dyslipidemic animal models were used to study the Meibomian gland and, more specifically, MGD [87][88][89]. To investigate whether systemic lipid disorders can be associated with DED and/or MGD, a study used three transgenic adult mice models, apolipoprotein-E knockout (APOE-KO), low-density lipoprotein receptor knockout (LDLR-KO) and a mouse model with overexpression of human apolipoprotein CIII (ApoCIIIKI), compared to age-and gender-matched C57BL/6 mice [87].…”

Section: Association Between Dyslipidemia and Mgdmentioning

confidence: 99%

“…Apolipoprotein E knockout (ApoE −/− ) mice are characterized by a marked increase in total plasma cholesterol levels and develop microvasculature lesions; making ApoE −/− mice a possible model for studying the mechanisms of hyperlipidemia and atherosclerosis in MGD and DED [91]. Recently, Bu et al [89] found that ApoE −/− mice present hypertrophic eyelids at 5 and 7 months of age, which was accompanied by Meibomian gland dropout and disordered acini and ducts in both upper and lower eyelids, when compared to age-matched control mice. These mice also present punctate corneal staining and signs of corneal damage, all clinical features of MGD [89].…”

Section: Association Between Dyslipidemia and Mgdmentioning

confidence: 99%

“…Recently, Bu et al [89] found that ApoE −/− mice present hypertrophic eyelids at 5 and 7 months of age, which was accompanied by Meibomian gland dropout and disordered acini and ducts in both upper and lower eyelids, when compared to age-matched control mice. These mice also present punctate corneal staining and signs of corneal damage, all clinical features of MGD [89]. Histological analysis of ApoE −/− mouse eyelids revealed plugging of the Meibomian gland orifice, duct dilation and heteromorphic acinar morphology.…”

Section: Association Between Dyslipidemia and Mgdmentioning

confidence: 99%

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Meibomian Gland Dysfunction: What Have Animal Models Taught Us?

Sun

Moreno

Dang

et al. 2020

IJMS

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Studies have estimated that currently 344 million people worldwide and 16.4 million adults in the US have some form of dry eye disease (DED). It is believed that approximately 70% of DED cases are due to some form of evaporative dry eye, for which Meibomian gland dysfunction (MGD) is the major cause. Unfortunately, currently there is no effective treatment for MGD, and solely palliative care is available. Given the importance of MGD in DED, there has been a growing interest in studying Meibomian gland development, homeostasis and pathology, and, also, in developing therapies for treating and/or preventing MGD. For such, animal models have shown to be a vital tool. Much of what is known today about the Meibomian gland and MGD was learnt from these important animal models. In particular, canine and rabbit models have been essential for studying the physiopathology and progression of DED, and the mouse model, which includes different knockout strains, has enabled the identification of specific pathways potentially involved in MGD. Herein, we provide a bibliographic review on the various animal models that have been used to study Meibomian gland development, Meibomian gland homeostasis and MGD, primarily focusing on publications between 2000 and 2020.

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