ArticleProceedings of the National Academy of Sciences of the United States of America2015
Poly(ADP-ribose) polymerase 1 is a novel target to promote axonal regeneration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- NADAntioxidants & redox signaling · 2023Review
- Role of NADCellular and molecular neurobiology · 2023Review
- Advances in molecular therapies for targeting pathophysiology in spinal cord injury.Expert opinion on therapeutic targets · 2023Review
- Rapid differentiation of hiPSCs into functional oligodendrocytes using an OLIG2 synthetic modified messenger RNA.Communications biology · 2022Article
- Epigenetic Modulation of Opioid Receptors by Drugs of Abuse.International journal of molecular sciences · 2022Review
- Poly(ADP-ribose) promotes toxicity ofScience translational medicine · 2022Article
- Sevoflurane exposure during the second trimester induces neurotoxicity in offspring rats by hyperactivation of PARP-1.Psychopharmacology · 2022Article
- Therapeutic Potentials of Poly (ADP-Ribose) Polymerase 1 (PARP1) Inhibition in Multiple Sclerosis and Animal Models: Concept Revisiting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Existing Evidence for the Repurposing of PARP-1 Inhibitors in Rare Demyelinating Diseases.Cancers · 2022Review
- Poly (ADP-ribose) polymerases as PET imaging targets for central nervous system diseases.Frontiers in medicine · 2022Review
- Avoid the trap: Targeting PARP1 beyond human malignancy.Cell chemical biology · 2021Review
- Gene set enrichment analysis and protein-protein interaction network analysis after sciatic nerve injury.Annals of translational medicine · 2020Article
- Cocaine-regulated microRNA miR-124 controls poly (ADP-ribose) polymerase-1 expression in neuronal cells.Scientific reports · 2020Article
- Effects of NADBiomolecules · 2020Review
- Poly(ADP-Ribose) Polymerase-3 Regulates Regeneration in Planarians.International journal of molecular sciences · 2020Article
- Selenium-Doped Carbon Quantum Dots Efficiently Ameliorate Secondary Spinal Cord Injury via Scavenging Reactive Oxygen Species.International journal of nanomedicine · 2020Article
- Dihydronicotinamide riboside is a potent NADThe Journal of biological chemistry · 2019Article
- Perspectives of RAS and RHEB GTPase Signaling Pathways in Regenerating Brain Neurons.International journal of molecular sciences · 2018Review
- Dual Inhibitors of PARPs and ROCKs.ACS omega · 2018Article
- Nicotinamide Adenine Dinucleotide Metabolism and Neurodegeneration.Antioxidants & redox signaling · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Therapeutic options for the restoration of neurological functions after acute axonal injury are severely limited. In addition to limiting neuronal loss, effective treatments face the challenge of restoring axonal growth within an injury environment where inhibitory molecules from damaged myelin and activated astrocytes act as molecular and physical barriers. Overcoming these barriers to permit axon growth is critical for the development of any repair strategy in the central nervous system. Here, we identify poly(ADP-ribose) polymerase 1 (PARP1) as a previously unidentified and critical mediator of multiple growth-inhibitory signals. We show that exposure of neurons to growth-limiting molecules--such as myelin-derived Nogo and myelin-associated glycoprotein--or reactive astrocyte-produced chondroitin sulfate proteoglycans activates PARP1, resulting in the accumulation of poly(ADP-ribose) in the cell body and axon and limited axonal growth. Accordingly, we find that pharmacological inhibition or genetic loss of PARP1 markedly facilitates axon regeneration over nonpermissive substrates. Together, our findings provide critical insights into the molecular mechanisms of axon growth inhibition and identify PARP1 as an effective target to promote axon regeneration.
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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 OpenQuestion graph.