Diabetic retinopathy (DR), the most common complication of diabetes mellitus, is the leading cause of visual impairment and blindness among working-age adults. Vision loss in DR can be caused by macular edema as the consequence of increased vascular permeability due to the blood-retinal barrier (BRB) breakdown and altered fluid movements into retinal tissue. Proliferative diabetic retinopathy (PDR), characterized by neovascularization on the retinal surface, can cause severe vision loss caused by vitreous hemorrhage and/or traction retinal detachment. In addition, accumulating data suggest that retinal neurodegeneration is an early component of DR, which can precede visible microvascular abnormalities. Increasing evidence points to inflammation as one of the key players in mediating diabetes-induced adverse effects on the neuronal and vascular components of the retina. Chronic, low-grade subclinical inflammation has been demonstrated to be involved in promoting BRB breakdown in diabetes. In patients, the most compelling evidence that inflammatory processes play an important role in DR pathogenesis is the dramatic effect of corticosteroids on diabetic macular edema. In addition to leukocytes, retinal glial cell dysfunction plays a major role in DR. Müller cells, the main glial cells of the retina, and microglial cells, the resident macrophages of the retina, are rapidly activated to release increased levels of proinflammatory mediators. The surgically excised fibrovascular membranes from patients with PDR are composed of new blood vessels, leukocytes, and a-smooth muscle actin-expressing myofibroblasts. In addition, several studies demonstrated the overexpression of angiogenic, inflammatory and fibrogenic factors in the ocular microenvironment of patients with PDR reinforcing the paradigm that inflammation, neovascularization, and fibrosis are critical mechanisms for PDR initiation and progression.
In this Research Topic we aim to gather preclinical and clinical studies that document the involvement of inflammation, and its specific cells, receptors, and signaling molecules, in the pathophysiology of DR. In addition, the role and guidelines of anti-inflammatory pharmacologic treatments will be discussed. We welcome the submission of different types of articles (e.g. Reviews, Mini-Reviews, and Original Research articles) covering the following topics in the context of diabetic retinopathy:
• Transcription factors in inflammatory reactions.
• Role of adhesion molecules and leukostasis in vascular cell death, breakdown of the BRB and capillary occlusion.
• Role of glial cell activation.
• Role of matrix metalloproteinases.
• Role of proinflammatory cytokines and chemokines.
• Role of oxidative stress and mitochondrial dysfunction.
• Role of signaling molecules of the inflammatory response in the pathogenesis of PDR angiogenesis and fibrosis.
• Anti-inflammatory strategies in the treatment of DR.
Diabetic retinopathy (DR), the most common complication of diabetes mellitus, is the leading cause of visual impairment and blindness among working-age adults. Vision loss in DR can be caused by macular edema as the consequence of increased vascular permeability due to the blood-retinal barrier (BRB) breakdown and altered fluid movements into retinal tissue. Proliferative diabetic retinopathy (PDR), characterized by neovascularization on the retinal surface, can cause severe vision loss caused by vitreous hemorrhage and/or traction retinal detachment. In addition, accumulating data suggest that retinal neurodegeneration is an early component of DR, which can precede visible microvascular abnormalities. Increasing evidence points to inflammation as one of the key players in mediating diabetes-induced adverse effects on the neuronal and vascular components of the retina. Chronic, low-grade subclinical inflammation has been demonstrated to be involved in promoting BRB breakdown in diabetes. In patients, the most compelling evidence that inflammatory processes play an important role in DR pathogenesis is the dramatic effect of corticosteroids on diabetic macular edema. In addition to leukocytes, retinal glial cell dysfunction plays a major role in DR. Müller cells, the main glial cells of the retina, and microglial cells, the resident macrophages of the retina, are rapidly activated to release increased levels of proinflammatory mediators. The surgically excised fibrovascular membranes from patients with PDR are composed of new blood vessels, leukocytes, and a-smooth muscle actin-expressing myofibroblasts. In addition, several studies demonstrated the overexpression of angiogenic, inflammatory and fibrogenic factors in the ocular microenvironment of patients with PDR reinforcing the paradigm that inflammation, neovascularization, and fibrosis are critical mechanisms for PDR initiation and progression.
In this Research Topic we aim to gather preclinical and clinical studies that document the involvement of inflammation, and its specific cells, receptors, and signaling molecules, in the pathophysiology of DR. In addition, the role and guidelines of anti-inflammatory pharmacologic treatments will be discussed. We welcome the submission of different types of articles (e.g. Reviews, Mini-Reviews, and Original Research articles) covering the following topics in the context of diabetic retinopathy:
• Transcription factors in inflammatory reactions.
• Role of adhesion molecules and leukostasis in vascular cell death, breakdown of the BRB and capillary occlusion.
• Role of glial cell activation.
• Role of matrix metalloproteinases.
• Role of proinflammatory cytokines and chemokines.
• Role of oxidative stress and mitochondrial dysfunction.
• Role of signaling molecules of the inflammatory response in the pathogenesis of PDR angiogenesis and fibrosis.
• Anti-inflammatory strategies in the treatment of DR.
