# Prostaglandin E1 in ischemic retinal diseases: mechanisms, evidence, and clinical perspectives

**Authors:** Dario Rusciano, Caterina Gagliano, Alessandro Avitabile, José Fernando Maya-Vetencourt

PMC · DOI: 10.3389/fmed.2026.1749690 · Frontiers in Medicine · 2026-02-09

## TL;DR

Prostaglandin E1 shows promise for treating ischemic retinal diseases by improving blood flow and protecting retinal cells, but more research is needed to confirm its effectiveness.

## Contribution

The paper reviews the mechanisms, preclinical evidence, and clinical potential of PGE1 in ischemic retinal diseases, highlighting new therapeutic approaches and delivery methods.

## Key findings

- PGE1 improves retinal perfusion and reduces oxidative stress in preclinical models.
- Early clinical trials suggest PGE1 may benefit visual outcomes and microcirculation with acceptable safety.
- Delivery challenges and small study sizes limit current evidence for PGE1 in retinal diseases.

## Abstract

Ischemic retinal diseases, including retinal vein and artery occlusions, diabetic retinopathy, and non-arteritic ischemic optic neuropathy, are major causes of vision loss worldwide and remain incompletely addressed by current therapies. Prostaglandin E1 (PGE1) has emerged as a promising therapeutic candidate due to its unique pharmacological profile, encompassing vasodilation, anti-thrombotic and rheological effects, endothelial protection, anti-inflammatory activity, and potential neuroprotective and mitochondrial benefits. Preclinical studies demonstrate that PGE1 improves retinal perfusion, reduces oxidative stress and edema, and promotes neuronal survival, while early clinical experiences, though limited in size, suggest favorable effects on visual outcomes and microcirculation, with an acceptable safety profile. However, evidence is limited by small sample sizes, heterogeneity, and delivery challenges. Emerging approaches, including sustained-release formulations, intravitreal delivery, and combination therapies, along with imaging biomarkers for patient selection, offer avenues to optimize clinical translation. While early clinical experiences—particularly in acutely treated central retinal artery occlusion—suggest potential benefits on retinal perfusion and visual outcomes, the current evidence remains limited by small, heterogeneous, and predominantly non-randomized studies. Consequently, PGE₁ should be regarded as an investigational or adjunctive approach, warranting further evaluation in well-designed, controlled clinical trials before any routine clinical adoption.

## Linked entities

- **Chemicals:** Prostaglandin E1 (PubChem CID 5280723), PGE1 (PubChem CID 5280723)
- **Diseases:** retinal vein occlusion (MONDO:0006951), retinal artery occlusion (MONDO:0006948), diabetic retinopathy (MONDO:0005266)

## Full-text entities

- **Genes:** EREG (epiregulin) [NCBI Gene 2069] {aka EPR, ER, Ep}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, COX2 (cytochrome c oxidase subunit II) [NCBI Gene 4513] {aka COII, MTCO2}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, NGF (nerve growth factor) [NCBI Gene 4803] {aka Beta-NGF, HSAN5, NGFB}, PTGER2 (prostaglandin E receptor 2) [NCBI Gene 5732] {aka COX-2, EP2}, ANGPT2 (angiopoietin 2) [NCBI Gene 285] {aka AGPT2, ANG2, LMPHM10}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, COX8A (cytochrome c oxidase subunit 8A) [NCBI Gene 1351] {aka COX, COX8, COX8-2, COX8L, MC4DN15, VIII}, HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}, CAMP (cathelicidin antimicrobial peptide) [NCBI Gene 820] {aka CAP-18, CAP18, CRAMP, FALL-39, FALL39, HSD26}, PTGER4 (prostaglandin E receptor 4) [NCBI Gene 5734] {aka EP4, EP4R}, HIF1A (hypoxia inducible factor 1 subunit alpha) [NCBI Gene 3091] {aka HIF-1-alpha, HIF-1A, HIF-1alpha, HIF1, HIF1-ALPHA, MOP1}, EPO (erythropoietin) [NCBI Gene 2056] {aka DBAL, ECYT5, EP, MVCD2}
- **Diseases:** headache (MESH:D006261), ischemic and neovascular retinal disorders (MESH:D015861), inflammation (MESH:D007249), excitotoxic injury (MESH:D014947), optic-disc edema (MESH:D010211), peripheral vascular disease (MESH:D016491), platelet aggregation (MESH:D001791), optic neuropathy (MESH:D009901), cerebral ischemic (MESH:D002547), Visual loss (MESH:D014786), mitochondrial damage (MESH:D028361), vascular occlusion (MESH:D008641), diabetes (MESH:D003920), cerebral and cardiac ischemia (MESH:D002545), endothelial dysfunction (MESH:D014652), AMD (MESH:D008268), edema (MESH:D004487), bleeding (MESH:D006470), hypoxic (MESH:D002534), uveitis (MESH:D014605), diabetic microangiopathy (MESH:D003925), hyperemia (MESH:D006940), hypotension (MESH:D007022), ischemia (MESH:D007511), blindness (MESH:D001766), venous stasis (MESH:D054070), veno-occlusive disease (MESH:D006504), hypoxia (MESH:D000860), systemic sclerosis (MESH:D012595), ischemic optic neuropathy (MESH:D018917), reperfusion injury (MESH:D015427), flushing (MESH:D005483), thrombotic (MESH:D013927), RVO (MESH:D012170), reactive Muller gliosis (MESH:D005911), microvascular degeneration (MESH:D017566), hypertension (MESH:D006973), arterial occlusion (MESH:D001157), demyelination (MESH:D003711), atherosclerosis (MESH:D050197), vascular dilation (MESH:D002311), diabetic macular edema (MESH:D008269), DR (MESH:D003930), ischemic stroke (MESH:D002544), ischemic retinal conditions (MESH:D012173), ischemic damage (MESH:D017202), ischemic and vascular disorders (MESH:D002561), erectile dysfunction (MESH:D007172), retinal ganglion cell degeneration (MESH:D012162), inflammatory cytokines (MESH:D000080424), neuronal degeneration (MESH:D009410), calcium (MESH:D002128), cardiac (MESH:D006331), Ischemic retinal diseases (MESH:D012164), crush (MESH:D003444), ocular disorders (MESH:D005128), amaurotic eyes (MESH:D013661), tissue (MESH:D017695), axonal injury (MESH:D001480), Central retinal artery occlusion (MESH:D015356)
- **Chemicals:** oxygen (MESH:D010100), prostaglandin (MESH:D011453), aspirin (MESH:D001241), glutamate (MESH:D018698), 13,14-dihydro-15-keto-PGE1 (MESH:C036808), -steroidal anti-inflammatory drugs (-), citicoline (MESH:D003566), Fluorescein (MESH:D019793), brimonidine (MESH:D000068438), PGE1 (MESH:D000527), steroids (MESH:D013256), lipid (MESH:D008055), minocycline (MESH:D008911), PLGA (MESH:D000077182), ROS (MESH:D017382)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Rodentia (rodent, order) [taxon 9989], Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12926496/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12926496/full.md

## References

76 references — full list in the complete paper: https://tomesphere.com/paper/PMC12926496/full.md

---
Source: https://tomesphere.com/paper/PMC12926496