ArticleStroke and vascular neurology2025
Delta opioid peptide [D-ala2, D-leu5]-Enkephalin's ability to enhance mitophagy via TRPV4 to relieve ischemia/reperfusion injury in brain microvascular endothelial cells.
Article in Stroke and vascular neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Delta-opioid receptor-mediated neural protection and regeneration.Neural regeneration research · 2026Article
- Herkinorin Exerted Neuroprotective Effects After Spinal Cord Injury by Suppression of NF-κB Pathway Activation.Neurochemical research · 2026Article
- NIR-II Imaging-Guided Photothermal Activation of a TRPV4-Targeted Nanoplatform Delivering Cycloastragenol to Promote Microglia Reprogramming and α-Synuclein Clearance in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitophagy Activation via the YAP/Parkin Pathway Underlies the Neuroprotective Action of Tetramethylpyrazine in Cerebral Ischemia/Reperfusion Injury.Biomolecules · 2026Article
- The role of TRPV4 in ischemic stroke.Molecular brain · 2026Review
- Polygalasaponin F alleviates cerebral ischemia-reperfusion injury through inhibiting mitophagy.Metabolic brain disease · 2025Article
- Long Neuro-COVID-19: Current Mechanistic Views and Therapeutic Perspectives.Biomolecules · 2024Review
- Advances in pathogenesis and treatment of vascular endothelial injury-related diseases mediated by mitochondrial abnormality.Frontiers in pharmacology · 2024Review
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8 authors.
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Abstract
backgroundLocal brain tissue can suffer from ischaemia/reperfusion (I/R) injury, which lead to vascular endothelial damage. The peptide δ opioid receptor (δOR) agonist [D-ala2, D-leu5]-Enkephalin (DADLE) can reduce apoptosis caused by acute I/R injury in brain microvascular endothelial cells (BMECs).
objectiveThis study aims to explore the mechanism by which DADLE enhances the level of mitophagy in BMECs by upregulating the expression of transient receptor potential vanilloid subtype 4 (TRPV4).
methodsBMECs were extracted and made to undergo oxygen-glucose deprivation/reoxygenation (OGD/R) accompanied by DADLE. RNA-seq analysis revealed that DADLE induced increased TRPV4 expression. The CCK-8 method was used to assess the cellular viability; quantitative PCR (qPCR) was used to determine the mRNA expression of
resultsWhen compared with the OGD/R group, OGD/R+DADLE group showed significantly enhanced cellular viability; increased expression of TRPV4, Beclin-1, LC3-II/I, PINK1 and Parkin; decreased p62 expression; a marked rise in calcium influx; further increases in mitophagy, an increase in ATP synthesis and an elevation of mitochondrial membrane potential. These protective effects of DADLE can be blocked by a TRPV4 inhibitor HC067047 or RNAi of TRPV4.
conclusionDADLE can promote mitophagy in BMECs through TRPV4, improving mitochondrial function and relieving I/R injury.
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