20.500.12556/RUL-136698 New insights into the role of cysteine cathepsins in neuroinflammation Neuroinflammation, which is mediated by microglia and astrocytes, is associated with the progression of neurodegenerative diseases. Increasing evidence shows that activated microglia induce the expression and secretion of various lysosomal cathepsins, particularly during the early stage of neuroinflammation. This trigger signaling cascade that aggravate neurodegeneration. To date, most research on neuroinflammation has focused on the role of cysteine cathepsins, the largest cathepsin family. Cysteine cathepsins are primarily responsible for protein degradation in lysosomes; however, they also play a role in regulating a number of other important physiological and pathological processes. This review focuses on the functional roles of cysteine cathepsins in the central nervous system during neuroinflammation, with an emphasis on their roles in the polarization of microglia and neuroinflammation signaling, which in turn causes neuronal death and thus neurodegeneration. microglia cysteine cathepsins neurotoxic polarization neuroinflammation neurodegeneration mikroglija cisteinski katepsini nevrotoksična polarizacija nevrovnetje nevrodegeneracija katepsini nevrodegenerativne bolezni true false true Angleški jezik Slovenski jezik Članek v reviji 2022-05-16 14:56:40 2022-05-16 14:56:43 2022-09-15 04:14:12 0000-00-00 00:00:00 2021 0 0 21 str. iss. 12, art. 1796 Vol. 11 2021 0000-00-00 Zaloznikova Objavljeno NiDoloceno 0000-00-00 0000-00-00 0000-00-00 577.152.34:616.831-003.8 2218-273X 10.3390/biom11121796 87903491 biomolecules-11-01796-v2.pdf biomolecules-11-01796-v2.pdf 1 73A728EBBAA8FCFAFE2F71EA6B250B04 9d107a6e422811ab2c7dc097eed5a4d5b30ac12a2b0244f298cd3374bc69fa06 e0cf258d-d517-11ec-8aca-00155dcfd717 https://repozitorij.uni-lj.si/Dokument.php?lang=slv&id=156445 https://www.mdpi.com/2218-273X/11/12/1796 1 85b99415-d517-11ec-8aca-00155dcfd717 https://repozitorij.uni-lj.si/Dokument.php?lang=slv&id=156444 Fakulteta za farmacijo 0 0 0