Next Article in Journal
Repositioning Dequalinium as Potent Muscarinic Allosteric Ligand by Combining Virtual Screening Campaigns and Experimental Binding Assays
Next Article in Special Issue
P2 × 7 Receptor Inhibits Astroglial Autophagy via Regulating FAK- and PHLPP1/2-Mediated AKT-S473 Phosphorylation Following Kainic Acid-Induced Seizures
Previous Article in Journal
Diversity and Antimicrobial Activity of Endophytic Fungi Isolated from Chloranthus japonicus Sieb in Qinling Mountains, China
Review

Microglial Phagocytosis—Rational but Challenging Therapeutic Target in Multiple Sclerosis

1
Neuron-Glia Biology in Health and Disease, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, 1649-003 Lisboa, Portugal
2
Department of Biochemistry and Human Biology, Faculty of Pharmacy, Universidade de Lisboa, 1649-003 Lisboa, Portugal
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(17), 5960; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21175960
Received: 1 August 2020 / Revised: 12 August 2020 / Accepted: 17 August 2020 / Published: 19 August 2020
(This article belongs to the Collection Neuroinflammatory Processes in Neurodegenerative Diseases)
Multiple sclerosis (MS) is the most common autoimmune and demyelinating disease of the central nervous system (CNS), characterized, in the majority of cases, by initial relapses that later evolve into progressive neurodegeneration, severely impacting patients’ motor and cognitive functions. Despite the availability of immunomodulatory therapies effective to reduce relapse rate and slow disease progression, they all failed to restore CNS myelin that is necessary for MS full recovery. Microglia are the primary inflammatory cells present in MS lesions, therefore strongly contributing to demyelination and lesion extension. Thus, many microglial-based therapeutic strategies have been focused on the suppression of microglial pro-inflammatory phenotype and neurodegenerative state to reduce disease severity. On the other hand, the contribution of myelin phagocytosis advocating the neuroprotective role of microglia in MS has been less explored. Indeed, despite the presence of functional oligodendrocyte precursor cells (OPCs), within lesioned areas, MS plaques fail to remyelinate as a result of the over-accumulation of myelin-toxic debris that must be cleared away by microglia. Dysregulation of this process has been associated with the impaired neuronal recovery and deficient remyelination. In line with this, here we provide a comprehensive review of microglial myelin phagocytosis and its involvement in MS development and repair. Alongside, we discuss the potential of phagocytic-mediated therapeutic approaches and encourage their modulation as a novel and rational approach to ameliorate MS-associated pathology. View Full-Text
Keywords: demyelinating lesions; microglia; myelin phagocytosis; multiple sclerosis; therapeutic strategies demyelinating lesions; microglia; myelin phagocytosis; multiple sclerosis; therapeutic strategies
Show Figures

Figure 1

MDPI and ACS Style

Pinto, M.V.; Fernandes, A. Microglial Phagocytosis—Rational but Challenging Therapeutic Target in Multiple Sclerosis. Int. J. Mol. Sci. 2020, 21, 5960. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21175960

AMA Style

Pinto MV, Fernandes A. Microglial Phagocytosis—Rational but Challenging Therapeutic Target in Multiple Sclerosis. International Journal of Molecular Sciences. 2020; 21(17):5960. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21175960

Chicago/Turabian Style

Pinto, Maria V.; Fernandes, Adelaide. 2020. "Microglial Phagocytosis—Rational but Challenging Therapeutic Target in Multiple Sclerosis" Int. J. Mol. Sci. 21, no. 17: 5960. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21175960

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop