Actin(g) toward a revised understanding of the role of cytoskeletal dynamics in neuronal bioenergetics

Neurons are energy-demanding cells.Disruptions in energy metabolism can quickly interrupt neuronal function,leading to cell death and neurodegeneration.For instance,ischemia rapidly depletes adenosine triphosphate(ATP)thereby disrupting energy-dependent cellular processes crucial for homeostasis,and axon degeneration is preceded by a collapse of axonal ATP levels.

Lin28 as a therapeutic target for central nervous system regeneration and repair

Axon disconnection in the central nervous system(CNS) usually causes signal transduction failure and severe functional deficits in patients with neurological disorders. Currently, there is no cure for patients with CNS axon injury and they usually suffer from life-long neurological defects(e.g., paralysis, loss of sensory function, and autonomic dysfunction) and life-threatening complications(e.g., autonomic dysreflexia).

Metabolic reprogramming of glial cells as a new target for central nervous system axon regeneration

After central nervous system(CNS)injury,severed axons fail to regenerate and their disconnections to the original targets result in permanent functional deficits in patients(Mahar and Cavalli,2018).Both the diminished intrinsic regenerative capacity of mature neurons and the inhibitory CNS milieu contribute to the regenerative failure following CNS injury.