Effect of ranibizumab on diabetic retinopathy via the vascular endothelial growth factor/STAT3/glial fibrillary acidic protein pathway DOI

Y.-C. Lin,

Jian Tan,

Yulin Tao

et al.

World Journal of Diabetes, Journal Year: 2025, Volume and Issue: 16(5)

Published: April 24, 2025

BACKGROUND Diabetic retinopathy (DR) is the leading cause of vision loss in patients with diabetes. The vascular endothelial growth factor (VEGF) pathway plays a critical role pathogenesis DR, and ranibizumab, an anti-VEGF agent, has shown promise its treatment. Signal transducer activator transcription 3 (STAT3) involved inflammatory processes cellular signaling, while glial fibrillary acidic protein (GFAP) marker cell activation, both contributing to retinal damage DR. However, mechanisms by which ranibizumab affect early-stage DR through VEGF/STAT3/GFAP are not fully understood. AIM To investigate early via pathway. METHODS Adult pigment epithelial 19 (ARPE-19) cells human microvascular (HRMECs) were cultured under high-glucose conditions simulate diabetic environment. effects on cytokine mRNA expression analyzed quantitative polymerase chain reaction Western blot analysis. A rat model was induced streptozotocin (60 mg/kg). Retinal changes, including ganglion (RGC) apoptosis, alterations, expression, evaluated using fundus fluorescein angiography, hematoxylin eosin periodic acid Schiff staining, immunofluorescence, confocal imaging, RESULTS High-glucose significantly increased levels VEGF, STAT3, GFAP, other cytokines ARPE-19 HRMECs. these partially suppressed ranibizumab. RGC leakage, elevated observed during rats. Ranibizumab treatment rats reduced restored RGCs, repaired networks. CONCLUSION Intravitreal modulates pathway, suppresses promotes repair, effectively delaying or preventing progression.

Language: Английский

Effect of ranibizumab on diabetic retinopathy via the vascular endothelial growth factor/STAT3/glial fibrillary acidic protein pathway DOI

Y.-C. Lin,

Jian Tan,

Yulin Tao

et al.

World Journal of Diabetes, Journal Year: 2025, Volume and Issue: 16(5)

Published: April 24, 2025

BACKGROUND Diabetic retinopathy (DR) is the leading cause of vision loss in patients with diabetes. The vascular endothelial growth factor (VEGF) pathway plays a critical role pathogenesis DR, and ranibizumab, an anti-VEGF agent, has shown promise its treatment. Signal transducer activator transcription 3 (STAT3) involved inflammatory processes cellular signaling, while glial fibrillary acidic protein (GFAP) marker cell activation, both contributing to retinal damage DR. However, mechanisms by which ranibizumab affect early-stage DR through VEGF/STAT3/GFAP are not fully understood. AIM To investigate early via pathway. METHODS Adult pigment epithelial 19 (ARPE-19) cells human microvascular (HRMECs) were cultured under high-glucose conditions simulate diabetic environment. effects on cytokine mRNA expression analyzed quantitative polymerase chain reaction Western blot analysis. A rat model was induced streptozotocin (60 mg/kg). Retinal changes, including ganglion (RGC) apoptosis, alterations, expression, evaluated using fundus fluorescein angiography, hematoxylin eosin periodic acid Schiff staining, immunofluorescence, confocal imaging, RESULTS High-glucose significantly increased levels VEGF, STAT3, GFAP, other cytokines ARPE-19 HRMECs. these partially suppressed ranibizumab. RGC leakage, elevated observed during rats. Ranibizumab treatment rats reduced restored RGCs, repaired networks. CONCLUSION Intravitreal modulates pathway, suppresses promotes repair, effectively delaying or preventing progression.

Language: Английский

Citations

0