Key result
CpG postconditioning after reperfusion limits scar size and preserves cardiac function by modulating inflammation.
Why the study?
Pharmacological postconditioning after myocardial infarction has been widely disappointing, motivating exploration of new pathways such as Toll-like receptor activation for myocardial postconditioning.
Hypothesis-generating in experimental MI; leaves open translation to clinical postconditioning after prior pharmacological failures.
Cytosine-phosphate-guanine (CpG) postconditioning seems to mediate inflammation via Toll-like receptor-1 and Toll-like receptor-9 signaling. Enhanced cytokine and chemokine expressions are partly attenuated by IL-10 and matrix metalloproteinase-8 (MMP8) induction, being associated with lower macrophage infiltration and M1-monocyte differentiation. Furthermore, switch from α- to β-MHC and balanced MMP/TIMP expression led to lesser cardiomyocyte apoptosis, smaller scar size, and preserved cardiac function. Data of pharmacological postconditioning have been widely disappointing to date. Our study suggests a new pathway promoting myocardial postconditioning via Toll-like receptor activation.
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Duerr et al. (2020) conducted a review in Myocardial infarction. CpG postconditioning was evaluated. CpG postconditioning after reperfused myocardial infarction modulates inflammation, reduces cardiomyocyte apoptosis, decreases scar size, and preserves cardiac function.
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