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. Author manuscript; available in PMC: 2016 Mar 31.
Published in final edited form as: J Am Coll Cardiol. 2015 Mar 31;65(12):1199–1214. doi: 10.1016/j.jacc.2015.01.031

Figure 7. Central Illustration. Cofilin in Cardiac Plaques: New Mechanisms for Dilated Cardiomyopathy.

Figure 7

Plaques- and tangle-like aggregates accumulate in the myocardium in some cases of iDCM. The actin depolymerizing protein cofilin is enriched in the aggregates together with its binding partners actin and MHCII. Cofilin is for the most phosphorylated, thus inactivated in iDCM. The prevalent inhibition of cofilin activity in conjunction with the damage to the myofibrillar integrity and the accumulation of fibrillar aggregates interfere with the proper function of the sarcomeres ultimately contributing to cardiac dysfunction in these cases of iDCM.