MEDLINE was accessed via Pub Med, and searched for published studies that analyzed MMP-9 and TIMP levels in patients with asymptomatic and symptomatic internal carotid stenosis and/or examined these parameters as potential risk markers for ischaemic stroke.
These results suggest that luteolin has potential in the treatment of ischemic stroke through inhibiting MMP9 and activating PI3K/Akt signaling pathway.
Variants in matrix metalloproteinase-9 gene are associated with hemorrhagic transformation in acute ischemic stroke patients with atherothrombosis, small artery disease, and cardioembolic stroke.
Our study provides preliminary evidence that the MMP9rs3918242 polymorphism is linked to a higher risk of IS, confirming the role of MMP9 in the pathophysiology of IS, with potentially important therapeutic implications.
TNF, NF-κB, IL-6, IL-1B, ICAM, and MMP-9 targets are all critical factors related to ischemic stroke, while the NF-κB signaling pathway, MAPK signaling pathway, TNF signaling pathway, and arachidonic acid metabolism play significant roles in the development of ischemic stroke.
Predictive value of plasma matrix metalloproteinase-9 concentrations for spontaneous haemorrhagic transformation in patients with acute ischaemic stroke: A cohort study in Chinese patients.
Blood-brain barrier (BBB) disruption detected on magnetic resonance imaging (MRI) in acute ischemic stroke as a hyperintense acute reperfusion marker (HARM) is associated with upregulation of matrix metalloproteinase-9 (MMP-9).
This study aimed to determine a possible association of mediators of inflammation and haemostasis (C-reactive protein, interleukin-6, matrix metalloproteinase-9, monocyte chemoattractant protein-1, asymmetric dimethylarginine [ADMA], symmetric dimethylarginine, von Willebrand factor and a disintegrin and metalloproteinase with a thrombospondin type 1 motif 13 [ADAMTS-13]) with the post-intervention grade of reperfusion, complications and clinical outcome in patients who underwent endovascular treatment of ischaemic stroke.
This meta-analysis showed that MMP-1 -1607 1G/2G and MMP-3 -1612 5A/6A were risk factors for ischemic stroke, while MMP-9-1562C/T was not associated with ischemic stroke.
Therefore, our meta-analysis suggested that MMP-9rs3918242 variants (T allele, TT and CT genotypes) contributed to significantly increase the risk of IS in the Chinese population.
Genotyping was performed using the Agena MassARRAY system, and chi-squared tests and genetic models were used to evaluate the associations between MMP-9 SNPs and the risk of IS.
The findings of this study suggest that the MMP9rs3918242 polymorphism is associated with an elevated risk of ischemic stroke and that this gene polymorphism interacts with BMI in the risk of ischemic stroke.
The aim of the present study was to investigate the association of six variants in MMP-9 gene with ischemic stroke severity and the risk for END in ischemic stroke (IS) patients with atrial fibrillation (AF).
Higher serum MMP-9 levels in the acute phase of ischemic stroke were associated with increased risk of mortality and major disability, suggesting that serum MMP-9 could be an important prognostic factor for ischemic stroke.
The following combinations of main keywords were used: ('Matrix Metalloproteinase' or 'MMP' or 'Stromelysin-1' or 'Gelatinase b') AND ('ischemic stroke' or 'IS') AND ('single nucleotide polymorphism' or 'gene polymorphism' or 'SNP').
In conclusion, our study suggests that MMP9rs3918242 polymorphism is correlated with an elevated risk of ischemic stroke, and this gene polymorphism has interaction with tobacco smoking in the risk of ischemic stroke.
According to the results of database retrieval systems and data analysis, MMP9 was predicted as a gene related to ischemic stroke and miR-212 is a potential regulating mRNA of MMP9.
Combination of rheumatoid factor, matrix metalloproteinase-9 and total homocysteine can improve the risk prediction of cognitive impairment among ischemic stroke patients with elevated blood pressure.
In the peripheral blood, numerous genes of inflammatory mediators, including MMP9, IL18RAP and GNLY, are altered in the acute phase of ischemic stroke.