ArticleInvestigative ophthalmology & visual science2025
Retinal Angiogenesis in Methamphetamine Self-Administration Rats.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Methamphetamine-Induced Loss of Syndecan-1 and Retinal Endothelial Integrity via the TAAR-1/MMP-9 Pathway.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Purpose: Given the evidence of a link between methamphetamine (METH) exposure and retinal vascular abnormalities, this study aims to investigate the molecular and cellular mechanisms underlying METH-induced retinal angiogenesis using a unique self-administration rat model and primary rat retinal microvascular endothelial cells (RRMECs). Method: To model the impact of compulsive use of METH, rats underwent an 8-week METH long-access self-administration protocol, with retinal tissues analyzed using whole retinal flatmount imaging and vascular network quantification. Proteomic analysis via liquid chromatography/tandem mass spectrometry identified differentially expressed proteins, while RRMECs were treated with METH to assess molecular changes through immunoblotting and quantitative RT-PCR. Results: Consistent with compulsive use of METH in humans and our previous experience with this model, rats self-administered high levels of METH. METH self-administration elevated dopamine levels in the vitreous humor and increased vascular density in both superficial and deep capillary layers across central, mid-peripheral, and peripheral retina regions. Proteomic analysis revealed 148 differentially expressed retinal proteins, with gene ontology enrichment highlighting pathways related to abiotic stimuli, hypoxia, and ischemia. Increased hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor a (VEGFa) expression confirmed a hypoxia-driven angiogenesis process, further supported by in vitro experiments showing enhanced endothelial cell proliferation and HIF-1α/VEGFa expression. Additionally, TAAR-1 upregulation in both the retina and endothelial cells was observed, with TAAR-1 antagonism reducing METH-induced endothelial cell proliferation and modulating HIF-1α/VEGFa signaling. Conclusions: METH self-administration leads to significant retinal vascular changes and angiogenesis, driven by upregulation of hypoxia-related pathways. TAAR-1 plays a critical role in endothelial cell proliferation through the HIF-1α/VEGFa pathway, potentially contributing to pathological retinal conditions.
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Registered trials
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