Fibrinolytic markers in coronary thrombi

Nordeng, Jostein; Helseth, R.; Åkra, S.; Hoffman, P.; Schandiz, H.; Roald, B.; Bendz, B.; Arnesen, H.; Solheim, S.; Seljeflot, I.

doi:10.1016/j.atherosclerosis.2022.06.785

Cited by 1 publication

(3 citation statements)

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“…We intravenously injected TNT to mice after AMI to reduce surgical trauma and TNT targeted the infarcted myocardium due to TA's strong affinity for cardiac ECM. The MMP2 level increased significantly 1 h after AMI [11] and TNT showed stimulated release of NPY in the presence of MMP2. The degradation of TIMP induced the influx of low pH and high ionic strength into the nanostructure in the myocardial infarction microenvironment and broke the hydrogen bonds and hydrophobic interactions between the TA and peptides.…”

Section: Discussionmentioning

confidence: 88%

“…MMP2 was three-fold higher in the heart 24 h after MI compared to the sham group (Figure 3E,F), which was consistent with previous reports. [11,12] The result indicated that the MMP2 was abundant in the infarcted microenvironment after myocardial infarction, which may be conducive to the release of TNT.…”

Section: Circulation Lifetime and Myocardial-infarction-targeting Cap...mentioning

confidence: 99%

“…Pro-Leu-Gly-Leu-Ala-Gly (PLGLAG) (TIMP) peptide was a competitive substrate of MMP2, which can respond to MMP2. [11] In this study, we fabricated a myocardial-infarction-targeted and infarcted microenvironment-responsive system based on TA and TIMP peptide. The therapeutic NPY loaded nanostructure (TNT) was used to reverse cardiac remodeling (Figure 1A).…”

Section: Introductionmentioning

confidence: 99%

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Targeted and Infarcted Microenvironment‐Responsive Peptide Therapeutics to Reverse Cardiac Remodeling

Qin

et al. 2022

Advanced Therapeutics

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Acute myocardial infarction (AMI) leads to cardiac remodeling and heart failure ultimately. However, the present therapeutic approaches show limited effects on restoring the blood supply quickly and controlling cardiac remodeling effectively. Here, a novel strategy for the repair of the injured heart by using tannic acid (TA) to deliver the therapeutic Neuropeptide Y (NPY), which is bio-responsively released by the incorporation of matrix metalloproteinase cleavable peptide Pro-Leu-Gly-Leu-Ala-Gly (TIMP), is developed. The NPY-loaded nanostructure, designated as TNT (TA/NPY/TIMP), is evaluated for its therapeutic effects on cardiac remodeling after AMI in mice. TNT specifically targets to infarcted tissues and releases NPY in the AMI environment with abundant matrix metalloproteinase 2. Interestingly, it is found that TNT attenuates early post-MI cardiac remodeling via increasing angiogenesis and the transition of M1 macrophages to M2 phenotype. This work contributes to developing a novel strategy for the recovery of cardiac functions after AMI.

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Section: Discussionmentioning

confidence: 88%

Section: Circulation Lifetime and Myocardial-infarction-targeting Cap...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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