Lysophospholipid Signaling Molecules in Fundus Neovascular Diseases
- 1Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong Kong, Shantou 515041, China
- 2Fifth Clinical Institute of Shantou University Medical College, Shantou 515041, China
- 3Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong SAR 999077, China
Abstract
Fundus neovascular diseases (FNDs) are vision-threatening ocular disorders featuring pathological neovascularization and pose a major global threat to vision health. Their pathogenesis is heterogeneous, involving multiple factors and pathways. Current clinical pharmacotherapies only target a limited range of molecular pathways via narrow mechanisms, leading to frequent suboptimal responses and disease recurrence, which restricts further therapeutic improvement for FNDs. Recent studies demonstrate that lysophospholipid signaling molecules selectively activate multiple cell-surface receptors, including G protein-coupled receptors, triggering multilayered downstream signaling cascades that govern neovascular initiation and progression. Aberrant activation of this endogenous signaling axis may underpin the limited efficacy of existing anti-angiogenic therapies, and its roles in pathological neovascularization have attracted intensive research attention. This review addresses three representative lysophospholipid mediators: lysophosphatidic acid, lysophosphatidylcholine, and sphingosine-1-phosphate. We systematically summarize their metabolic routes, receptor binding profiles, downstream signaling networks, and pro-angiogenic mechanisms. We also discuss the current research status and translational potential of targeting lysophospholipid axes as innovative therapies, aiming to provide theoretical and translational evidence for developing precise pathway-directed interventions.
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BibTeX
@article{zhou2026lysophospholipid,
title = {{Lysophospholipid Signaling Molecules in Fundus Neovascular Diseases}},
author = {Xinbei Zhou and Shaolang Chen and Jiajian Liang and Junchao Chen and Hongan Hu and Wai Kit Chu and Qingping Liu and Changzhen Fu},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms272110025},
url = {https://www.mdpi.com/1422-0067/27/21/10025},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Lysophospholipid Signaling Molecules in Fundus Neovascular Diseases
AU - Xinbei Zhou
AU - Shaolang Chen
AU - Jiajian Liang
AU - Junchao Chen
AU - Hongan Hu
AU - Wai Kit Chu
AU - Qingping Liu
AU - Changzhen Fu
PY - 2026
DA - 2026/11/09
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms272110025
UR - https://www.mdpi.com/1422-0067/27/21/10025
AB - Fundus neovascular diseases (FNDs) are vision-threatening ocular disorders featuring pathological neovascularization and pose a major global threat to vision health. Their pathogenesis is heterogeneous, involving multiple factors and pathways. Current clinical pharmacotherapies only target a limited range of molecular pathways via narrow mechanisms, leading to frequent suboptimal responses and disease recurrence, which restricts further therapeutic improvement for FNDs. Recent studies demonstrate that lysophospholipid signaling molecules selectively activate multiple cell-surface receptors, including G protein-coupled receptors, triggering multilayered downstream signaling cascades that govern neovascular initiation and progression. Aberrant activation of this endogenous signaling axis may underpin the limited efficacy of existing anti-angiogenic therapies, and its roles in pathological neovascularization have attracted intensive research attention. This review addresses three representative lysophospholipid mediators: lysophosphatidic acid, lysophosphatidylcholine, and sphingosine-1-phosphate. We systematically summarize their metabolic routes, receptor binding profiles, downstream signaling networks, and pro-angiogenic mechanisms. We also discuss the current research status and translational potential of targeting lysophospholipid axes as innovative therapies, aiming to provide theoretical and translational evidence for developing precise pathway-directed interventions.
SN - 1422-0067
ER -