ArticleMolecular therapy : the journal of the American Society of Gene Therapy2026
Stress-induced mitochondrial fragmentation in endothelial cells disrupts blood-retinal barrier integrity causing neurodegeneration.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- From Adaptive Resilience to Catastrophic Systems Collapse: Endothelial Entropy, Ferroptotic Propagation, and the Maternal Point of No Return in Emergency Peripartum Hysterectomy.International journal of molecular sciences · 2026Review
- A DPEP1-Binding and mitochondria-targeted nanocomposite relieves acute respiratory distress syndrome by inhibiting Drp1-mediated mitochondria fission.Materials today. Bio · 2026Article
- Calcium at the Helm: Mechanisms and Therapeutic Targets in the Retinal Neurovascular Unit.Biomolecules · 2026Review
- Intraocular pressure induced blood retinal barrier compromise in mouse models and human glaucoma.Nature communications · 2026Article
- Age-Related Neurovascular Dysfunction in the Retina and Potential Pathogenic Mechanisms.Investigative ophthalmology & visual science · 2026Review
- Sex differences in human umbilical vein endothelial cells following ox-LDL injury.Biology of sex differences · 2026Article
- The key mechanisms and intervention strategies of cell-type-specific mitochondrial metabolism in ophthalmic diseases.Frontiers in cell and developmental biology · 2026Review
- Nrf2/HO-1 signaling in retinal neurodegenerative diseases: redox homeostasis, cytoprotection, and therapeutic perspectives.Frontiers in medicine · 2026Review
- Endothelial metabolic zonation in the vascular network: a spatiotemporal blueprint for angiogenesis.American journal of physiology. Heart and circulatory physiology · 2025Review
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Increased vascular leakage and endothelial cell (EC) dysfunction are major features of neurodegenerative diseases. Here, we investigated the mechanisms leading to EC dysregulation and asked whether altered mitochondrial dynamics in ECs impinge on vascular barrier integrity and neurodegeneration. We show that ocular hypertension, a major risk factor for developing glaucoma, induced mitochondrial fragmentation in retinal capillary ECs, accompanied by increased oxidative stress and ultrastructural defects. Analysis of EC mitochondrial components revealed overactivation of dynamin-related protein 1 (DRP1), a central regulator of mitochondrial fission, during glaucomatous damage. Pharmacological DRP1 inhibition or EC-specific in vivo gene delivery of a dominant-negative DRP1 mutant was sufficient to rescue mitochondrial volume, reduce vascular leakage, and increase expression of the tight junction claudin-5 (CLDN5). We further demonstrate that EC-targeted CLDN5 gene augmentation restored blood-retinal barrier integrity, promoted neuronal survival, and improved light-evoked visual behaviors in glaucomatous mice. Our findings reveal that preserving mitochondrial homeostasis and EC function are valuable strategies to enhance neuroprotection and improve vision in glaucoma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.