ArticleScientific reports2025
siRNA-mediated inhibition of NTT-MMP-2 reduces oxidative stress and apoptotic signaling in an ex vivo model of ischemia/reperfusion injury.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Matrix metalloproteinase-2 (MMP-2), particularly its N-terminally truncated isoform (NTT-MMP-2), plays a pivotal role in cardiac ischemia-reperfusion (I/R) injury. NTT-MMP-2 is induced by oxidative stress and activates both pro-inflammatory and pro-apoptotic pathways as well as an innate immune response within the cell. This study investigated the involvement of NTT-MMP-2 in oxidative stress, inflammation, and cardiomyocyte injury, focusing on its mitochondrial activity. Using an ex vivo Langendorff-perfused rat heart model, we demonstrated that I/R significantly increased mitochondrial NTT-MMP-2 activity, total ROS/RNS production, and markers of cardiac injury, including lactate dehydrogenase activity (LDH), and reduced cardiac mechanical function. NTT-MMP-2 activity and cytochrome c positively correlated with nuclear factor kappa B (NF-κB) expression and LDH activity, while negatively correlating with heart rate and rate pressure product (cytochrome c), suggesting NTT-MMP-2 involvement in mitochondrial dysfunction and apoptotic signaling. Partial inhibition of MMP-2 with siRNA reduced NTT-MMP-2 activity, preserved cardiac function, and decreased cytochrome c and NF-κB levels, although it paradoxically increased NFATc1 and IL-6 expression. These findings indicate that while NTT-MMP-2 contributes to oxidative and inflammatory damage during IRI, it may not be the sole regulator of innate immune activation. Moreover, IL-6 upregulation following MMP-2 silencing may reflect a compensatory cardioprotective response. This study identifies NTT-MMP-2 as a potential therapeutic target in ischemic heart disease, with siRNA-based strategies offering partial protection against I/R injury through modulation of mitochondrial stress and apoptosis pathways.
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