Diyabetik Retinopati ve Diyabetik Maküla Ödeminde Patogenez
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Tarih
2018
Yazarlar
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Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Diabetik retinopatinin (DR) patogenezi vasküler, inflamatuar ve nöronal mekanizmaları içeren karmaşık bir yapıdadır. Diabet retinada metabolik ve fizyolojik anomalilere neden olur ancak bunların diyabetik retinopatinin bilinen bulgularının gelişimine ne kadar katkısı olduğu aşikar değildir. Anjiyogenez ve inflamasyonun hastalığın patogenezi ile ilişkili olduğu gösterilmiştir. Hiperglisemi ve hipoksi tarafından tetiklenen moleküler mediatörler ve beraberindeki metabolik yolaklar doğrudan endotel hücrelerine etki ederek artmış vasküler geçirgenlik, endotel hücreleri arasındaki bağlantıların bozulması, lökostaz ve sonunda diyabetik maküler ödeme (DMÖ) neden olabilir. Moleküler mediatörler ve matabolik yolaklar arasındaki etkileşim, sinyal iletimi ve geri besleme mekanizmaları oldukça karmaşıktır ve tam olarak anlaşılamamıştır. Bu derlemede DR ve DMÖ gelişiminde rol oynayan mekanizmalar mikrovasküler ve moleküler seviyede ele alınmıştır.
The pathogenesis of diabetic retinopathy (DR) is complex and several vascular, inflammatory and neuronal mechanisms are involved. Diabetes causes a number of metabolic and physiologic abnormalities in the retina, but which of these abnormalities contribute to recognized features of DR is less clear. Angiogenesis and inflammation have been shown to be involved in the pathogenesis of this disease. Molecular mediators, acting in conjunction with metabolic pathways, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, leukostasis and ultimately diabetic macular edema (DME). The interactions, signalling events and feedback loops between the various molecular mediators and metabolic pathways are complicated and are not completely understood. The underlying mechanisms of DR and DME, on both microvascular and molecular levels, are discussed in this review.
The pathogenesis of diabetic retinopathy (DR) is complex and several vascular, inflammatory and neuronal mechanisms are involved. Diabetes causes a number of metabolic and physiologic abnormalities in the retina, but which of these abnormalities contribute to recognized features of DR is less clear. Angiogenesis and inflammation have been shown to be involved in the pathogenesis of this disease. Molecular mediators, acting in conjunction with metabolic pathways, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, leukostasis and ultimately diabetic macular edema (DME). The interactions, signalling events and feedback loops between the various molecular mediators and metabolic pathways are complicated and are not completely understood. The underlying mechanisms of DR and DME, on both microvascular and molecular levels, are discussed in this review.
Açıklama
Anahtar Kelimeler
Diyabetik retinopati, Diyabetik maküler ödem, Patogenez, Diabetic retinopathy, Diabetic macular edema, Pathogenesis.
Kaynak
Güncel Retina Dergisi
WoS Q Değeri
Scopus Q Değeri
Cilt
2
Sayı
2
