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作者

Fu-shin X. Yu Patrick S.Y. Lee Lingling Yang Nan Gao Yangyang Zhang Alexander V. Ljubimov Ellen Yang Qingjun Zhou Lixin Xie

作者单位

Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, 60064, USA Departments of Ophthalmology and Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, 48201, USA State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, China Departments of Biomedical Sciences and Neurosurgery, Cedars-Sinai Medical Center, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

刊名

Progress in Retinal and Eye Research

年份

2022

页码

101039

ISSN

1350-9462

关键词

Corneal wound healing Diabetic keratopathy Diabetic peripheral nerve degeneration

摘要

Diabetic peripheral neuropathy is the most common complication of diabetes, with several underlying pathophysiological mechanisms, some of which are still uncertain. The cornea is an avascular tissue and sensitive to hyperglycemia, resulting in several diabetic corneal complications including delayed epithelial wound healing, recurrent erosions, neuropathy, loss of sensitivity, and tear film changes. The manifestation of DPN in the cornea is referred to as diabetic neurotrophic keratopathy . Re...更多

Diabetic peripheral neuropathy is the most common complication of diabetes, with several underlying pathophysiological mechanisms, some of which are still uncertain. The cornea is an avascular tissue and sensitive to hyperglycemia, resulting in several diabetic corneal complications including delayed epithelial wound healing, recurrent erosions, neuropathy, loss of sensitivity, and tear film changes. The manifestation of DPN in the cornea is referred to as diabetic neurotrophic keratopathy . Recent studies have revealed that disturbed epithelial-neural-immune cell interactions are a major cause of DNK. The epithelium is supplied by a dense network of sensory nerve endings and dendritic cell processes, and it secretes growth/neurotrophic factors and cytokines to nourish these neighboring cells. In turn, sensory nerve endings release neuropeptides to suppress inflammation and promote epithelial wound healing, while resident immune cells provide neurotrophic and growth factors to support neuronal and epithelial cells, respectively. Diabetes greatly perturbs these interdependencies, resulting in suppressed epithelial proliferation, sensory neuropathy, and a decreased density of dendritic cells. Clinically, this results in a markedly delayed wound healing and impaired sensory nerve regeneration in response to insult and injury. Current treatments for DPN and DNK largely focus on managing the severe complications of the disease. Cell-based therapies hold promise for providing more effective treatment for diabetic keratopathy and corneal ulcers.收起

文献类型

期刊