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. 2008 Nov 14;296(1):H1–H12. doi: 10.1152/ajpheart.00995.2008

Table 2.

TLR signaling modulates myocardial I/R injury and remodeling

Mice Infarct Models Effects in Knockout Mice References
TLR2−/−
I/R (30′ I/60 R′) Smaller infarct sizes, reduced neutrophil recruitment, reduced ROS and cytokines 35
Permanent coronary ligation Improved survival rate, attenuated remodeling, but same infarct sizes at 4 wk 136
TLR4
    C57 BL/10 ScCr C3H/HeJ I/R (60′ I/24 h R) Smaller infarct sizes, reduced MPO activity and complement 3 deposition 118
    C3H/HeJ I/R (60′ I/120′ R) Smaller infarct sizes, decreased cardiac expression of TNF, MCP-1, and ILs 28
    C3H/HeJ I/R (60′ I/24 h R) Smaller infarct sizes, but no gain in LV function 75
    WT with eritoran I/R (30′ I/120′ R) Smaller infarct sizes, reduced pJNK, reduced cytokine expression 134
    C3H/HeJ Permanent coronary ligation Reduced LV remodeling, improved systolic function, reduced cytokine expression 149
    C57 BL/10 ScCr Permanent coronary ligation Improved LV function on day 6 after infarction, improved survival rate, reduced LV remodeling and apoptosis at 4 wk. 125
MyD88−/− I/R (30′ I/24 h R) Smaller infarct sizes, improved LV function, and attenuated cytokine expression and neutrophil recruitment 36

TLR, Toll-like receptor; ROS, reactive oxygen species; MPO, myeloperoxidase; MCP-1, monocyte chemoattractant protein-1; pJNK, phosphorylated JNK; MyD88, myeloid differentiation primary-response gene 88.