Matrix metaloproteinases in neurological brain lesions: A new therapeutic target?

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Introduction. Matrix metalloproteinases (MMP) are a family of proteolytic enzymes that degrade the extracellular matrix and are found in a large amount of human tissues. Their main functions are to maintain the integrity of the extracellular matrix, to modulate the interaction of the cells during development, to contribute to tissue remodeling, to directly participate in angiogenesis and to facilitate cellular migration. Due to the importance of its maintaining extracellular matrix function, MMP expression is tightly regulated at transcriptional level, through proform activation and with the binding to tissular inhibitors. Despite this complex regulation system, MMP regulation can be altered, producing an overexpression of these proteolytic proteins that alter the tissular structure, possibly destroying the tissue, as observed in some neurologic pathologies such as multiple sclerosis, aneurism formation and cerebral ischemia. The role that MMP have in traumatic brain lesions is almost unknown and is derived mainly from in vivo and in vitro experimental studies, and only from three papers performed in humans. There are some experimental studies that relate the brain alterations produced after traumatic brain injury with an increase in the concentration of various MMP. Aim. To review the role of these proteases in human brain lesions, emphasizing on the function of these proteases in traumatic brain injury lesions and their possible therapeutic target. Development. A bibliographic search was performed on Medline database. Conclusions. Some MMP could be related to blood-brain barrier alteration and postraumatic edema formation, turning them into promising therapeutic targets. © 2010 Revista de Neurología.
Original languageEnglish
Pages (from-to)95-107
JournalRevista de Neurologia
Issue number2
Publication statusPublished - 16 Jul 2010


  • Blood-brain barrier
  • Cerebral ischemia
  • Extracellular matrix
  • Matrix metalloproteinases
  • Neuroinflammation
  • Traumatic brain injury


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