Myocardial remodelling involves not only the myocytes, but also non-myocyte cells and the extracellular matrix, which constitutes around 6 % of the normal heart and includes fluid, collagen and glycoproteins. In non-ischaemic dilated cardiomyopathy (DCM), the cardiac interstitium increases as a result of diffuse interstitial (microscopic) fibrosis, post-necrotic replacement (macroscopic) fibrosis or myocardial oedema. The activation of the renin–angiotensin–aldosterone system is a major determinant of fibroblasts activation and collagen deposition, with the transforming growth factor β as the downstream signal mediator. Endomyocardial biopsy still represents the current reference method for interstitial and replacement myocardial fibrosis assessment, but cardiovascular magnetic resonance (CMR) allows in vivo detection of macroscopic fibrosis with post-contrast late enhancement imaging. Moreover, recent pre- and post-contrast T1 mapping techniques provide a quantitative estimation of myocardial interstitial remodelling, with potential diagnostic and prognostic clinical utility. Here, we review the pathophysiological mechanisms of myocardial interstitial remodelling in DCM, its non-invasive characterization with biomarkers and with CMR, as well as the most recent studies about their clinical utility.