The role of non-protein coding RNAs (ncRNAs), microRNAs (miRNAs) in particular, as fine-tuners of both pathological and physiological processes is no longer a matter of debate. With the recent discovery of miRNAs in a wide variety of body fluids and considering them as tools employed in horizontal gene transfer between cells, a new horizon opens in the field of diagnosis and therapeutics. Circulating miRNAs not only enable the communication among cells, but also provide insight into the pathological and physiological state of the originating cells. In this review we summarize the recent advances made in this field, arguing for compelling translation of miRNAs into clinical practice. Moreover, we provide overview of their characteristics and how they impact the evolution of tumor microenvironment and cell-to-cell communication, advancing the idea that miRNAs may function as hormones.

The death of retinal ganglion cells (RGCs) is a key factor in the pathophysiology of all types of glaucoma, but the mechanism of pathogenesis of glaucoma remains unclear. RGCs are a group of central nervous system (CNS) neurons whose soma are in the inner retina. The axons of RGCs form the optic nerve and converge at the optic chiasma; from there, they project to the visual cortex via the lateral geniculate nucleus (LGN). In recent years, there has been increasing interest in the dysfunction and death of CNS and retinal neurons caused by transneuronal degeneration of RGCs, and the view that glaucoma is a widespread neurodegenerative disease involving CNS damage appears more and more frequently in the literature. In this review, we summarize the current knowledge of LGN and visual cortex neuron damage in glaucoma and possible mechanisms behind the damage. This review presents an updated and expanded view of neuronal damage in glaucoma, and reveals new and potential targets for neuroprotection and treatment.

Radiation-induced optic neuropathy (RION) is a devastating complication following external beam radiation therapy (EBRT) that leads to acute vision loss. To date, no efficient, available treatment for this complication, due partly to the lack of understanding regarding the developmental processes behind RION. Here, we report radiation caused changes in mitochondrial dynamics by regulating the mitochondrial fission proteins dynamin-related protein 1 (Drp1) and fission-1 (Fis1). Concurrent with an excessive production of reactive oxygen species (ROS), both neuronal injury and visual dysfunction resulted. Further, our findings delineate an important mechanism by which cyclin-dependent kinase 5 (Cdk5)-mediated phosphorylation of Drp1 (Ser616) regulates defects in mitochondrial dynamics associated with neuronal injury in the development of RION. Both the pharmacological inhibition of Cdk5 by roscovitine and the inhibition of Drp1 by mdivi-1 inhibited mitochondrial fission and the production of ROS associated with radiationinduced neuronal loss. Taken together, these findings may have clinical significance in preventing the development of RION.