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This editorial refers to ‘Ultrastructural remodelling of Ca2+ signalling apparatus in failing heart cells’ by H.-D. Wu et al ., pp. 430–438, this issue. Cardiac remodelling, often defined as changes in the mass and shape of the whole heart,1 has been a focus of research over several decades. Despite considerable efforts, the cellular and molecular mechanisms that lead to contractile dysfunction of the remodelled heart are still not clear. Remodelling may also occur at the level of the cardiomyocyte and is then termed ultrastructural remodelling. Studies have revealed substantial ultrastructural alterations in several parts of the cardiomyocytes during cardiac disease, including the sarcoplasmic reticulum (SR)2 and transverse (T)-tubules,3,4 and in the positioning of ion channels and pumps that are crucial in regulating myocardial contraction and relaxation. Thus, it is likely that ultrastructural remodelling can explain several important aspects of systolic and diastolic heart failure of various aetiologies.The machinery that couples the electrical activation of the cardiomyocyte to mechanical contraction is set to control transient rises of [Ca2+] in the cytosol. Research in the past decades has revealed that the global rise of [Ca2+] in the cytosol that activates myofilaments is regulated by mechanisms that are confined within spatially constrained microdomains in the cardiomyocyte. These microdomains occur at sites where Ca2+ channels in the T-tubule membrane come very close to Ca …

Calcium release units in heart failure: that's about the size of it