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Aqueous Humor Angiotensin-Converting Enzyme and TGF-β1 Levels in Proliferative Vitreoretinopathy: A Prospective
Nurullah Koçak1, Ahmet Özdemir1, Mertcan Esenkaya1
1Ondokuzmayıs University Hospital, Department of Ophthalmology, Atakum, 55200, Samsun, Turkey.
Retina (Philadelphia, Pa.)
|May 19, 2026
Summary
Elevated aqueous transforming growth factor-β1 (TGFβ1) is linked to proliferative vitreoretinopathy (PVR) in patients with retinal detachment. Angiotensin-converting enzyme (ACE) elevation is associated with retinal detachment but not specifically PVR.
Area of Science:
- Ophthalmology
- Biochemistry
Background:
- Proliferative vitreoretinopathy (PVR) is a severe complication of rhegmatogenous retinal detachment (RRD).
- Understanding the molecular mechanisms underlying PVR is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate plasma and aqueous humor levels of angiotensin-converting enzyme (ACE) and transforming growth factor-β1 (TGFβ1) in patients with PVR secondary to RRD.
- To determine the association of these biomarkers with the presence and severity of PVR.
Main Methods:
- Eighty-eight patients were categorized into three groups: RRD with PVR, RRD without PVR, and healthy controls.
- Plasma and aqueous humor samples were analyzed for ACE and TGFβ1 concentrations using ELISA.
- Statistical analyses, including regression and ROC analyses, were performed to assess biomarker associations with PVR.
Main Results:
- Aqueous TGFβ1 levels were significantly elevated in the PVR group compared to non-PVR and control groups.
- Aqueous ACE levels were higher in both RRD groups (PVR and non-PVR) than in controls, but did not differ between RRD groups.
- Aqueous TGFβ1 showed high discriminative performance for PVR, and was identified as an independent predictor, along with symptom duration.
Conclusions:
- Aqueous TGFβ1 is a significant biomarker associated with PVR in RRD.
- Elevated aqueous ACE levels appear to be a consequence of RRD rather than a specific indicator of PVR.
- These findings highlight the potential role of TGFβ1 as a therapeutic target for PVR.
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