ReviewFrontiers in cellular neuroscience2017
Multifaceted Roles of Metzincins in CNS Physiology and Pathology: From Synaptic Plasticity and Cognition to Neurodegenerative Disorders.
Review in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Integrated Systems Analysis Deciphers Transcriptome and Glycoproteome Links in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- Craniofacial and olfactory sensory changes after long-term unilateral nasal obstruction-an animal study using MMP-3-LUC transgenic rats.Scientific reports · 2024Article
- Dynamic regulation of the extracellular matrix in reward memory processes: a question of time.Frontiers in cellular neuroscience · 2023Review
- Integrins Bidirectionally Regulate the Efficacy of Inhibitory Synaptic Transmission and Control GABAergic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Kynurenine Pathway Metabolites as Biomarkers in Alzheimer's Disease.Disease markers · 2022Review
- Leptolysin, aFrontiers in cellular and infection microbiology · 2022Article
- Extracellular Metalloproteinases in the Plasticity of Excitatory and Inhibitory Synapses.Cells · 2021Review
- Multifaceted Role of Matrix Metalloproteinases in Neurodegenerative Diseases: Pathophysiological and Therapeutic Perspectives.International journal of molecular sciences · 2021Review
- Metalloproteinases and Their Inhibitors: Potential for the Development of New Therapeutics.Cells · 2020Review
- Matrix Metalloproteinase 14 Mediates APP Proteolysis and Lysosomal Alterations Induced by Oxidative Stress in Human Neuronal Cells.Oxidative medicine and cellular longevity · 2020Article
- Thiamine deficiency contributes to synapse and neural circuit defects.Biological research · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular matrix (ECM) and membrane proteolysis play a key role in structural and functional synaptic plasticity associated with development and learning. A growing body of evidence underscores the multifaceted role of members of the metzincin superfamily, including metalloproteinases (MMPs), A Disintegrin and Metalloproteinases (ADAMs), A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTSs) and astacins in physiological and pathological processes in the central nervous system (CNS). The expression and activity of metzincins are strictly controlled at different levels (e.g., through the regulation of translation, limited activation in the extracellular space, the binding of endogenous inhibitors and interactions with other proteins). Thus, unsurprising is that the dysregulation of proteolytic activity, especially the greater expression and activation of metzincins, is associated with neurodegenerative disorders that are considered synaptopathies, especially Alzheimer's disease (AD). We review current knowledge of the functions of metzincins in the development of AD, mainly the proteolytic processing of amyloid precursor protein, the degradation of amyloid β (Aβ) peptide and several pathways for Aβ clearance across brain barriers (i.e., blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB)) that contain specific receptors that mediate the uptake of Aβ peptide. Controlling the proteolytic activity of metzincins in Aβ-induced pathological changes in AD patients' brains may be a promising therapeutic strategy.
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