Research progress on the crosstalk disorders between local and systemic metabolism based on the physiological hypoxic characteristics of meibomian glands

Authors:Ren Yaoyao, Liu Yang

Corresponding author: Liu Yang, Email:drliuyang_eye@whu.edu.cn

Published:2026-10-10

DOI:10.3760/cma.j.cn115989-20260306-00094


ABSTRACT 

Meibomian gland dysfunction (MGD) is the leading cause of evaporative dry eye. Epidemiological evidence indicates a significantly higher prevalence of MGD among populations with metabolic diseases, suggesting a profound intrinsic connection between them. This review utilizes the unique anatomical microenvironment of the meibomian gland as its core entry point: the acini are completely avascular, and all nutrients must reach acinar cells via diffusion across the basement membrane. The resulting physiological hypoxic microenvironment constitutes a structural basis for understanding meibomian gland metabolism. Building upon this, the article systematically elucidates the pathophysiological mechanisms by which systemic metabolic disorders impair meibomian gland function across four dimensions: glycation-induced thickening of the basement membrane and the subsequent strengthening of the diffusion barrier; Abnormalities in circulating lipid profiles leading to deterioration of meibum quality; Paracrine injury driven by chronic low-grade inflammation and peri-acinar microvascular lesions. This review posits that meibomian gland function is closely linked to systemic metabolic health, and incorporating MGD into the spectrum of ocular complications of metabolic syndrome has significant theoretical and clinical value.

KEYWORDS:

Meibomian gland dysfunction;Metabolic syndrome;Physiological hypoxia;Diabetes mellitus;Dry eye;Meibum


COPYRIGHTS:

Copyright by Chinese Medical Association

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All articles published represent the opinions of the authors, and do not reflect the official policy of the Chinese Medical Association or the Editorial Board, unless this is clearly specified.


Authors Info & Affiliations 

Ren Yaoyao

Department of Ophthalmology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China

Liu Yang

Department of Ophthalmology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China


Figures & Tables

Figure 1 Pathophysiological mechanism by which the physiological hypoxic microenvironment of meibomian gland acini mediates systemic metabolic disorder–induced meibomian gland dysfunction TNF-α: tumor necrosis factor-α; IL: interleukin; pO₂: partial pressure of oxygen; ROS: reactive oxygen species; HIF-1α: hypoxia-inducible factor-1α; Gli1: zinc-finger transcription factor; PPARγ: peroxisome proliferator-activated receptor-γ


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