| Literature DB >> 33265917 |
Jessica Maiuolo1,2, Micaela Gliozzi1,2, Vincenzo Musolino1,2, Cristina Carresi1,2, Saverio Nucera1,2, Miriam Scicchitano1, Federica Scarano1,2, Francesca Bosco1,2, Francesca Oppedisano1,2, Roberta Macrì1,2, Vincenzo Mollace1,2,3.
Abstract
Oligodendrocytes are myelinating cells of the central nervous system which are generated by progenitor oligodendrocytes as a result of maturation processes. The main function of mature oligodendrocytes is to produce myelin, a lipid-rich multi-lamellar membrane that wraps tightly around neuronal axons, insulating them and facilitating nerve conduction through saltatory propagation. The myelination process requires the consumption a large amount of energy and a high metabolic turnover. Mitochondria are essential organelles which regulate many cellular functions, including energy production through oxidative phosphorylation. Any mitochondrial dysfunction impacts cellular metabolism and negatively affects the health of the organism. If the functioning of the mitochondria is unbalanced, the myelination process is impaired. When myelination has finished, oligodendrocyte will have synthesized about 40% of the total lipids present in the brain. Since lipid synthesis occurs in the cellular endoplasmic reticulum, the dysfunction of this organelle can lead to partial or deficient myelination, triggering numerous neurodegenerative diseases. In this review, the induced malfunction of oligodendrocytes by harmful exogenous stimuli has been outlined. In particular, the effects of alcohol consumption and heavy metal intake are discussed. Furthermore, the response of the oligodendrocyte to excessive mitochondrial oxidative stress and to the altered regulation of the functioning of the endoplasmic reticulum will be explored.Entities:
Keywords: alcohol; endoplasmic reticulum; heavy metals; myelination; oligodendrocytes; oxygen reactive species; unfolded protein response
Year: 2020 PMID: 33265917 DOI: 10.3390/biomedicines8120553
Source DB: PubMed Journal: Biomedicines ISSN: 2227-9059