Regular ArticleMetalloproteinase Inhibition Prevents Acute Respiratory Distress Syndrome☆
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Matrix metalloproteinase inhibitors prevent sepsis-induced refractoriness to vasoconstrictors in the cecal ligation and puncture model in rats
2015, European Journal of PharmacologyCitation Excerpt :Subsequent studies reinforced the ability of LPS and several other inflammatory mediators to induce an in vitro rapid release of MMP-9 in whole human blood (Pugin et al., 1999), comparable to the release of MMP-9 in the blood of healthy humans after LPS injection (Albert et al., 2003; Pugin et al., 1999). Inhibition of MMPs in vivo prevented the lung injury (Carney et al., 2001) and protected against the lethality associated with endotoxemia (Hu et al., 2005) and with the cecal ligation and puncture (CLP) model of sepsis in rats (Steinberg et al., 2003). Severe sepsis and septic shock involve an exacerbated inflammatory process and are accompanied by a progressive reduction in blood pressure, which is refractory to fluid infusion and vasoactive drugs and limits blood supply to peripheral and vital organs, contributing to multiple organ failure and the high rate of sepsis-associated mortality (for review see Dellinger, 2003).
Jack of all trades: Pleiotropy and the application of chemically modified tetracycline-3 in sepsis and the acute respiratory distress syndrome (ARDS)
2011, Pharmacological ResearchCitation Excerpt :Studies by the Nieman group have clearly shown the effects off COL-3 mediated MMP blockade in the context of ARDS. Carney et al. showed that COL-3 caused a decrease in MMP-2 and MMP-9 concentrations in the bronchoalveolar lavage fluid of pigs injured by cardiopulmonary bypass (CPB) combined with a very small dose of LPS infusion and pretreated with COL-3 [61] (Figs. 4 and 5). Note how COL-3 treatment reduces gelatinase and elastase activity to nearly that of naive controls in Fig. 5.
Matrix metalloproteinase inhibitor properties of tetracyclines: Therapeutic potential in cardiovascular diseases
2011, Pharmacological ResearchCitation Excerpt :We have observed that endotoxemia-induced vascular hypocontractility may be a result of increased MMP-2 activity to cleave intracellular smooth muscle contractile proteins [163] (Fig. 2). CMTs which lack antibacterial activity yet retain MMP inhibitory action were also examined in different sepsis models [70–72,164] and were shown to reduce pulmonary lesions and mortality. CMT-3 prevented lipopolysaccharide-induced lung injury [70,72] and systemic hypotension [70] in a porcine model of acute respiratory distress syndrome.
DLK1 overexpression improves sepsis-induced cardiac dysfunction and fibrosis in mice through the TGF-β1/Smad3 signaling pathway and MMPs
2023, Journal of Molecular Histology
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Presented at the Annual Meeting of the Association for Academic Surgery, Seattle, Washington, November 18–22, 1998, and winner of the Association of Academic Surgery Resident Research Award.
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