TIMP2 and TIMP3 knockout mouse models demonstrate differential roles in cardiac hypertrophy and fibrosis independent of MMP inhibition.
Hypothesis-generating for MMP-independent TIMP targeting in remodeling; leaves open translation to human HF therapies.
TIMP2 and TIMP3 play fundamental and differential roles in mediating pathological remodelling, independent from their MMP-inhibitory function. TIMP2(-/-) and TIMP3(-/-) mice provide a unique opportunity to study myocardial hypertrophy and fibrosis independently, and their impact on cardiac dysfunction.
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Dong et al. (2014) studied this question.
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