Nerve injury and regeneration

The paper identifies nicotinic acid mononucleotide (NaMN) as an allosteric inhibitor of SARM1 that promotes axonal protection by blocking NMN binding and stabilizing the inactive SARM1 conformation.

This study shows that overexpressing RTN3 promotes axon regeneration and functional recovery after CNS injury, dependent on protrudin.

The paper identifies chromatin accessible sites and transcription factors in RGCs that correlate with axon growth capacity and shows CREB overexpression promotes axon regeneration.

This study shows that astrocytes switch from a kinase-based to a calcium-based response to BDNF during development, with Kidins220/ARMS modulating both pathways and regulating Kir4.1 expression.

This study identifies the Piezo-Atr-Chek1-Cdc25 pathway as an inhibitory mechanism for axon regeneration, showing that disrupting it enhances regeneration in Drosophila and mammals.

This paper develops a novel scaffold biomaterial coated with extracellular matrix proteins to promote axonal regeneration after spinal cord injury.

This study shows ALKBH1 demethylates N6-mA in sensory neurons, promoting axon regeneration by regulating neurodevelopmental genes.

The paper shows that prenyl-Cdc42 mRNA localizes to PNS axons and promotes axon growth through localized translation and prenylation.

This study shows that the prion protein is not required for sciatic nerve regeneration after crush injury in mice.

The paper shows that restoring Schwann cell c-Jun rescues nerve regeneration failures in aging and chronic denervation by enhancing regenerative support.

This study shows that spinal cord injury (SCI) in dorsal column sensory neurons leads to downregulation of lipid metabolism genes, unlike sciatic nerve injury, which may hinder axon regeneration.

This study identifies efferocytosis as a key mechanism for nerve debridement following sciatic nerve injury through single-cell RNA-sequencing and genetic analysis.

This study identifies GSK-3β and Smad3 as key mediators of TGF-β1's anti-neuritogenic effects by modulating CRMP2 phosphorylation in sensory neurons.

The paper proposes using adult retina explants as an ex vivo model to study axon regeneration in the mature CNS, offering advantages over in vitro and in vivo approaches.

This study shows that ZDHHC17 couples DLK and NMNAT2 pathways to control both somal and distal axon degeneration after optic nerve crush.

This study uses optogenetics to activate ERK and AKT signaling in Drosophila, enhancing axon regeneration and functional recovery in both PNS and CNS.

This study identifies fatty acid synthesis in satellite glial cells as a mechanism promoting axon regeneration after nerve injury.

The paper shows that peripheral sensory neurons undergo consistent transcriptional changes after axonal injury, which promote regeneration but also suppress cell identity, with Atf3 playing a key role.

This study shows that inhibiting PTEN promotes axon regeneration in adult sensory neurons, particularly in IB4-positive neurons following peripheral axotomy.

The paper identifies axonal PIP3 deficiency as a cause of CNS regeneration failure and shows that p110δ can restore regeneration by acting hyperactively.

The paper shows that prenylation of axonally translated proteins is required for NGF-dependent axon growth in sympathetic neurons.

This study shows YAP/TAZ are necessary for Schwann cell remyelination but not proliferation after nerve injury, and their expression depends on axon regeneration.

This study shows that knocking out myosin IIA/B in retinal ganglion cells promotes optic nerve regeneration, with synergistic effects when combined with Lin28 overexpression.

This paper describes a porcine model for studying long-distance peripheral nerve regeneration, focusing on surgical techniques and outcomes for ultra-long regenerative distances.

This paper describes a mouse line with inducible Cre expression specifically targeting Remak Schwann cells, with partial neuronal depletion using Flpe.

The paper identifies Robo2 as a key regulator of target-selective peripheral nerve regeneration in response to glia-derived signals in zebrafish.

This study shows mitochondrial impairment triggers Wallerian-like axon degeneration by depleting NMNAT2, activating SARM1, and replicating key steps of the Wallerian pathway in mice and flies.

The paper measures catecholaminergic axon density in adult mice after brain injury and finds they regrow over weeks to months following controlled cortical impact or stab injury.

The paper identifies distinct phases of axon degeneration regulated by p75NTR and DR6, showing calcium flux and spheroid rupture as key events.

The paper identifies TERT and p53 as regulators of axon regeneration downstream of c-Myc in the CNS and PNS, showing p53 overexpression promotes regeneration.