Research progress of UWFFA and OCTA in retinal vein occlusion: A review

An, Weiting; Han, Jindong

doi:10.1177/11206721211027411

Cited by 6 publications

(2 citation statements)

References 41 publications

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“…MCP-1 belongs to the chemokine family. Its expression is increased by retinal hypoxia, atherosclerosis, and oxidative stress, and it promotes vascular endothelial activation, adhesion, induction of vascular endothelium, and overexpression of extravascular matrix, leading to vascular occlusion, which triggers the formation of microthrombi and neovascularization [12] . In the retina, MCP-1 can promote the phosphorylation of endothelial cell tight junction proteins, activate monocyte macrophages to produce inflammatory factors, such as TNF-α, disrupt the blood-retinal barrier, increase the permeability of the retinal vasculature, and cause abnormal fluid entry and exit, which then leads to ME.…”

Section: Mcp-1mentioning

confidence: 99%

Research Progress on Pathogenesis and Related Inflammatory Factors of Macular Edema Secondary to Retinal Vein Occlusion

2024

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Retinal vein occlusion (RVO) is a relatively common retinal vascular disease characterized by vascular obstruction due to thrombus from various causes, resulting in retinal hemorrhage, fluid exudation, and varying degrees of retinal hypoxia and ischemia, and its secondary macular edema (ME) is the main cause of patients' impaired vision. Retinal vein occlusion secondary to macular edema is a pathophysiological process involving multiple factors, with a complex pathogenesis and many cytokines involved, resulting in an imbalance of fluids entering and transferring out of the retina, which leads to the formation of ME [1] . In recent years, with the development of molecular biology techniques, inflammatory factors associated with RVO-ME have become an important aspect in the study of RVO-ME. In this paper, we review the inflammatory factors associated with retinal vein occlusion secondary to macular edema and the pathogenesis of RVO-ME.

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Section: Mcp-1mentioning

confidence: 99%

Research Progress on Pathogenesis and Related Inflammatory Factors of Macular Edema Secondary to Retinal Vein Occlusion

2024

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“…In recent years, the continued development of OCT has greatly increased its use in various scientific and clinical research fields. [14][15][16] Exploration of OCT in dermatology is already underway, focusing on skin repair or regeneration. [17][18][19] Furthermore, OCT-based angiography (OCTA) enables in vivo imaging of capillary blood flow and skin structural features, qualitatively and quantitatively assessing vascular responses to acute skin injuries, helping to determine wound severity and likely healing outcomes, potentially providing new insights into the pathophysiology and dynamics of skin diseases.…”

Section: Introductionmentioning

confidence: 99%

Basic fibroblast growth factor gel preparation induces angiogenesis during wound healing

Mou

et al. 2023

Int J Artif Organs

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Purpose: This study aimed to observe the effect of basic fibroblast growth factor (bFGF) gel preparation on wound repair in a full-thickness skin defect rat model and to further explore its mechanism. Methods: The full-thickness skin defect model of Wistar rats was created with circular wounds of 20 mm or 10 mm in diameter on both sides of the spine. The animals were divided into the normal, model, control gel, and bFGF gel groups (300 IU/cm2). The effects of the bFGF gel on wound healing were evaluated and compared. Optical coherence tomography (OCT)-based angiography (OCTA) was used to investigate the effects of bFGF on angiogenesis during wound healing. Western blotting, polymerase chain reaction (PCR), and enzyme-linked immunosorbent assay (ELISA) kits were used to detect the effect of the gel preparation on the levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMP2 and MMP9) on the wound surface to explore the mechanism. Results: The bFGF gel significantly reduced wound area, promoted the formation of wound granulation tissue, and accelerated wound healing in the bFGF gel group on days 7 and 14, compared with the control gel group. OCTA results showed that bFGF significantly improved wound vascular density, diameter, and circumference. Western blot, PCR, and ELISA results showed that the gel preparation could promote the expression levels of MMP2, MMP9, and VEGF on the wound surface 7 and 14 days after injury. Conclusion: bFGF promotes angiogenesis in wound areas. Topical gel preparations of bFGF can be developed for use in wound repair.

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