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. Author manuscript; available in PMC: 2016 Jul 1.
Published in final edited form as: Metalloproteinases Med. 2015 Oct 30;2:75–82. doi: 10.2147/MNM.S74093

Table 2.

Examples of applying the laws of MI thermodynamics to post-MI inflammation and extracellular matrix responses following matrix metalloproteinase-9 modulation

Law Example Insights gained
First: post-MI, the cardiac system remodels in
an attempt to maintain maximum LV function
MMP-9 deletion limits early inflammation to reduce
macrophage infiltration and ECM turnover, which
attenuate later collagen deposition and infarct expansion.
Early inflammation and ECM
turnover status predicts later
changes in LV structure or function.
Second: post-MI, the LV undergoes unidirectional
modifications that lead to irreversible
transformation in geometry and function
Macrophage-specific MMP-9 overexpression blunts pro-
inflammatory leukocyte phenotypes and prevents early
post-MI LV dysfunction without affecting cell numbers or
collagen deposition.
Cell-to-cell communication and
timing of intervention have major
effects on MI outcomes.
Third: post-MI, the infarct approaches scar
equilibrium over time
While day 28 post-MI inflammation in the infarct is
similar between wild-type and MMP-9 null mice, the
ECM continues to differentially remodel and the LV
operates at different levels of dysfunction.
End scar quality and LV function is
an ultimate outcome measurement.

Note: Data from references.22,2832

Abbreviations: MI, myocardial infarction; LV, left ventricle; MMP-9, matrix metalloproteinase-9; ECM, extracellular matrix.