Neuroinflammation and galectins: a key relationship in neurodegenerative diseases.
Eleazar Ramírez HernándezBeatriz Alanis OlveraDaniela Carmona GonzálezOscar Guerrero MarínDenisse Pantoja MercadoLucero Valencia GilLuis F Hernández-ZimbrónJosé Luis Sánchez SalgadoI Daniel LimónEdgar ZentenoPublished in: Glycoconjugate journal (2022)
Neurodegeneration is a pathological condition that is associated with the loss of neuronal function and structure. In neurodegenerative diseases, mounting evidence indicates that neuroinflammation is a common factor that contributes to neuronal damage and neurodegeneration. Neuroinflammation is characterized by the activation of microglia, the neuroimmune cells of the central nervous system (CNS), which have been implicated as active contributors to neuronal damage. Glycan structure modification is defining the outcome of neuroinflammation and neuronal regeneration; moreover, the expression of galectins, a group of lectins that specifically recognize β-galactosides, has been proposed as a key factor in neuronal regeneration and modulation of the inflammatory response. Of the different galectins identified, galectin-1 stimulates the secretion of neurotrophic factors in astrocytes and promotes neuronal regeneration, whereas galectin-3 induces the proliferation of microglial cells and modulates cell apoptosis. Galectin-8 emerged as a neuroprotective factor, which, in addition to its immunosuppressive function, could generate a neuroprotective environment in the brain. This review describes the role of galectins in the activation and modulation of astrocytes and microglia and their anti- and proinflammatory functions within the context of neuroinflammation. Furthermore, it discusses the potential use of galectins as a therapeutic target for the inflammatory response and remodeling in damaged tissues in the central nervous system.
Keyphrases
- cerebral ischemia
- inflammatory response
- lipopolysaccharide induced
- lps induced
- subarachnoid hemorrhage
- blood brain barrier
- brain injury
- stem cells
- induced apoptosis
- traumatic brain injury
- toll like receptor
- cell cycle arrest
- signaling pathway
- neuropathic pain
- immune response
- cell death
- multiple sclerosis
- wound healing
- endoplasmic reticulum stress
- cerebrospinal fluid