STOM Promotes Retinal Angiogenesis in Diabetic Retinopathy via the ERK1/2/VEGFA Pathway

Area of Science:

• Ophthalmology
• Endocrinology
• Molecular Biology

Background:

• Diabetic retinopathy (DR) is a major cause of blindness globally.
• The molecular mechanisms driving DR-associated retinal angiogenesis are not fully understood.

Purpose of the Study:

• To investigate the role of STOM in diabetic retinopathy-related retinal angiogenesis.
• To elucidate the signaling pathway involved in STOM's function in DR.

Main Methods:

• Utilized a streptozotocin-induced diabetic rat model and high glucose-treated human retinal microvascular endothelial cells (HRMECs).
• Assessed STOM, VEGFA, and ERK1/2 pathway molecule expression via qRT-PCR, WB, and IHC.
• Performed functional assays (proliferation, migration, tube formation) following STOM manipulation and pathway inhibition.

Main Results:

• STOM expression was significantly increased in diabetic rat retinas and high glucose-exposed HRMECs.
• STOM knockdown inhibited, while overexpression enhanced, HRMEC proliferation, migration, and angiogenesis.
• STOM promoted VEGFA upregulation and angiogenesis by activating the ERK1/2 signaling pathway.

Conclusions:

• STOM facilitates pathological retinal angiogenesis in diabetic retinopathy through the ERK1/2/VEGFA pathway.
• STOM represents a potential therapeutic target for managing diabetic retinopathy.