ArticleCell death & disease2021
AAV-mediated inhibition of ULK1 promotes axonal regeneration in the central nervous system in vitro and in vivo.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- The potential role of RhoA/ROCK-inhibition on locomotor recovery after spinal cord injury: a systematic review of in-vivo studies.Spinal cord · 2025Pooled it
- AAV-Driven miR-146a Promotes Neurite Outgrowth and Axonal Regeneration in Cortical Neurons.Journal of neurochemistry · 2026Article
- Impaired macroautophagy confers substantial risk for intellectual disability in children with autism spectrum disorders.Molecular psychiatry · 2025Article
- Genetic engineering frontiers in cell manipulation-based tissue engineering: A comprehensive review.BioImpacts : BI · 2025Review
- Biological engineering approaches for modulating the pathological microenvironment and promoting axonal regeneration after spinal cord injury.Frontiers in neuroscience · 2025Review
- AAV-Mediated Expression of miR-17 Enhances Neurite and Axon Regeneration In Vitro.International journal of molecular sciences · 2024Article
- Metabolomics reveals the effects of hydroxysafflor yellow A on neurogenesis and axon regeneration after experimental traumatic brain injury.Pharmaceutical biology · 2023Article
- Advances in molecular therapies for targeting pathophysiology in spinal cord injury.Expert opinion on therapeutic targets · 2023Review
- Autophagy and beyond: Unraveling the complexity of UNC-51-like kinase 1 (ULK1) from biological functions to therapeutic implications.Acta pharmaceutica Sinica. B · 2022Review
- Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Axonal damage is an early step in traumatic and neurodegenerative disorders of the central nervous system (CNS). Damaged axons are not able to regenerate sufficiently in the adult mammalian CNS, leading to permanent neurological deficits. Recently, we showed that inhibition of the autophagic protein ULK1 promotes neuroprotection in different models of neurodegeneration. Moreover, we demonstrated previously that axonal protection improves regeneration of lesioned axons. However, whether axonal protection mediated by ULK1 inhibition could also improve axonal regeneration is unknown. Here, we used an adeno-associated viral (AAV) vector to express a dominant-negative form of ULK1 (AAV.ULK1.DN) and investigated its effects on axonal regeneration in the CNS. We show that AAV.ULK1.DN fosters axonal regeneration and enhances neurite outgrowth in vitro. In addition, AAV.ULK1.DN increases neuronal survival and enhances axonal regeneration after optic nerve lesion, and promotes long-term axonal protection after spinal cord injury (SCI) in vivo. Interestingly, AAV.ULK1.DN also increases serotonergic and dopaminergic axon sprouting after SCI. Mechanistically, AAV.ULK1.DN leads to increased ERK1 activation and reduced expression of RhoA and ROCK2. Our findings outline ULK1 as a key regulator of axonal degeneration and regeneration, and define ULK1 as a promising target to promote neuroprotection and regeneration in the CNS.
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