ArticleJournal of nanobiotechnology2025
Mitochondria-targeted nanovesicles for ursodeoxycholic acid delivery to combat neurodegeneration by ameliorating mitochondrial dysfunction.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Hierarchical targeting biomimetic nanoparticles directing to lesion site and mitochondria promote neuroregeneration and attenuate inflammation after spinal cord injury.Materials today. Bio · 2026Article
- Research Advances on Organelle-Targeted Drug Delivery Systems for the Treatment of Brain Tumors and Central Nervous System Inflammation.Pharmaceutics · 2026Review
- The Road toward a Trojan Horse Malaria Vaccine: Chemical Augmentation of Live Sporozoites without Affecting Their Viability.Molecular pharmaceutics · 2026Article
- Mitophagy-mediated immune evasion: Shared strategies of pathogens.Redox biology · 2026Review
- Ursodeoxycholic acid mitigates cerebral ischemia/reperfusion injury by inhibiting thrombin-induced lipid peroxidation through activation of ALDH3A1.Redox biology · 2026Article
- Neuroprotective effects of ursodeoxycholic acid in Parkinson's disease and Alzheimer's disease.Neuroprotection (Chichester, England) · 2026Review
- The vicious cycle: unraveling the interplay between α-synuclein, mitochondrial dysfunction, and neuroinflammation in Parkinson's disease.Journal of neurology · 2026Review
- Neuroprotective effect of astrocytic dopamine Drd2 receptor on mitochondrial complex I in a mouse model of Parkinson's disease through β-arrestin2-NDUFA10 regulation.Cell death and differentiation · 2026Article
- Nanomaterial strategies for mitigating protein misfolding and neuroinflammation in neurodegenerative diseases.Zoological research · 2026Review
- Multifunctional Hybrid Nanomedicines for Neurodegenerative Diseases: A Paradigm Shift from Rational Design to Clinical Translation.International journal of nanomedicine · 2026Review
- Mitochondrial dysfunction in immune cells during the perioperative period: mechanisms, emerging therapeutic strategies, and implications for multi-organ protection.Frontiers in immunology · 2026Review
- Organelle-Targeted Nanotherapeutics for Parkinson's Disease: From Pathogenesis to Preclinical Strategies and Translational Challenges.International journal of nanomedicine · 2026Review
- Fucoidan Therapy for Extraintestinal Diseases: Targeting the Microbiota-Gut-Organ Axes.Biomolecules · 2025Review
- Cardiolipin and mitochondrial membrane integrity in neurodegeneration: insights from α-synuclein-driven Parkinson's disease.Acta neuropathologica communications · 2025Review
- Nanotechnology for Neurodegenerative Diseases: Recent Progress in Brain-Targeted Delivery, Stimuli-Responsive Platforms, and Organelle-Specific Therapeutics.International journal of nanomedicine · 2025Review
- Mitochondria-Targeted Nanosystems in the Treatment of Central Nervous System Diseases.International journal of nanomedicine · 2025Review
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13 authors.
Funding
Abstract
Mitochondria are pivotal in sustaining oxidative balance and metabolic activity within neurons. It is well-established that mitochondrial dysfunction constitutes a fundamental pathogenic mechanism in neurodegeneration, especially in the context of Parkinson's disease (PD), this represents a promising target for therapeutic intervention. Ursodeoxycholic acid (UDCA), a clinical drug used for liver disease, possesses antioxidant and mitochondrial repair properties. Recently, it has gained attention as a potential therapeutic option for treating various neurodegenerative diseases. However, multiple barriers, including the blood-brain barrier (BBB) and cellular/mitochondrial membranes, significantly hinder the efficient delivery of therapeutic agents to the damaged neuronal mitochondria. Macrophage-derived nanovesicles (NVs), which can traverse the BBB in response to brain inflammation signals, have demonstrated promising tools for brain drug delivery. Nevertheless, natural nanovesicles inherently lack the ability to specifically target mitochondria. Herein, artificial NVs are loaded with UDCA and then functionalized with triphenylphosphonium (TPP) molecules, denoted as UDCA-NVs-TPP. These nanovesicles specifically accumulate in damaged neuronal mitochondria, reduce oxidative stress, and enhance ATP production by 42.62%, thereby alleviating neurotoxicity induced by 1-methyl-4-phenylpyridinium (MPP+). Furthermore, UDCA-loaded NVs modified with TPP successfully cross the BBB and accumulate in the striatum of PD mice. These nanoparticles significantly improve PD symptoms, as demonstrated by a 48.56% reduction in pole climb time, a 59.09% increase in hanging ability, and the restoration of tyrosine hydroxylase levels to normal, achieving remarkable therapeutic efficacy. Our work highlights the immense potential of these potent UDCA-loaded, mitochondria-targeting nanovesicles for efficient treatment of PD and other central neurodegenerative diseases.
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