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Immune targets in myocardial remodeling merit exploration in dilated cardiomyopathy; leaves open clinical translation pending prospective trials.
Extracellular matrix (ECM) homeostasis is an important factor for normal cardiac structure and function. Synthesis of collagens is regulated at the cellular level, whereas collagen deposition depends on a balance between matrix metalloproteinases and tissue inhibitors of metalloproteinases. Immune-mediated regulation of myocardial collagen synthesis and deposition during inflammation remains unclear. It appears possible that a paracrine/autocrine action of cytokines on inflammatory and myocardial cells may lead to altered interstitial metabolism resulting in left ventricular remodelling and dysfunction. Efforts to delineate the interaction between immune cells, myocardial cells and ECM are important because chronic myocardial inflammation is recognized in dilated cardiomyopathy.
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Matthias Pauschinger (2002) studied this question.
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