Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy - PubMed
5 days ago
- #diabetic retinopathy
- #hyaluronan
- #angiogenesis
- Dysregulated hyaluronan (HA) metabolism contributes to inflammation and angiogenesis in proliferative diabetic retinopathy (PDR).
- Key enzymes and receptors in the HA pathway (HAS2, Hyal-1, Hyal-2, CD44, RHAMM) are upregulated in PDR vitreous samples and epiretinal membranes.
- Diabetes increases Hyal-1, CD44, RHAMM, and reactive oxygen species in rat retinas.
- Ultralow molecular weight HA (ULMW-HA) induces retinal vascular permeability and upregulates inflammatory and angiogenic markers in rats and Müller cells.
- Inhibitors of ERK1/2 and NF-κB pathways reduce ULMW-HA-induced upregulation of VEGF, angiopoietin-2, and MCP-1/CCL2.
- The hyaluronidase inhibitor apigenin reduces VEGF and MCP-1/CCL2 levels under diabetic conditions and mitigates monocyte adherence.
- Abnormal HA metabolism is linked to retinal endothelial dysfunction, driving PDR progression.