## 1 Introduction  
The extracellular matrix (ECM) plays a key role in multicellular organism development [1]. Previously, it was believed that the ECM was an inert component that solely served to provide mechanical stability, but today, it is viewed as a highly dynamic system that undergoes constant remodelling with post-translational modifications of its molecular components [2, 3]. The ECM is found within all tissues and organs and acts not only as a framework for cellular organelles but also has a crucial signal transduction role in both healthy and diseased tissues [2, 4]. The composition of the ECM is tissue specific and heterogeneous and its unique structure is formed early during tissue development. The ECM is comprised of many macromolecules that can be categorised into two key groups: **fibre-forming** and **non-fibre-forming** molecules. As the ECM is a highly organised ensemble of different macromolecules, even small changes to each subunit can have detrimental effects on the macromolecules' physiochemical properties and thus the properties of the tissue and the cellular phenotypes, ultimately resulting in functional changes [3].  
It is possible to identify changes in the ECM during disease. However, it is vital to distinguish between ECM changes causing disease and ECM changes that occur as a result of disease progression [3]. During the early stages of development and in response to injury, the remodelling rate of the ECM is increased and involves various molecules, including but not exclusively limited to, integrins and matrix metalloprotein (MMPs) [5] and also changes of intra- or extracellular tension forces [5]. There is an extensive list of diseases that involve disturbances of the ECM including: connective tissue disorders, genetic disorders, liver cirrhosis, inflammatory bowel disease, chronic kidney disease and several cardiovascular diseases [3; 6]. In cardiovascular diseases, preserving ECM integrity by reducing excess fibrosis or inhibiting degradation is a critical target of both treatment and prevention strategies [7]. Given the critical role of the extracellular matrix in both physiological homeostasis and pathological compensatory processes, the ECM has become an attractive new target for molecular imaging with applications in numerous diseases.  
The ECM can be imaged using both invasive (including tissue staining methods, nonlinear optic microscopy, electron microscopy and fluorescence life time imaging [8; 9; 10]) and non-invasive including [MRI (magnetic resonance imaging), PET (positron emission tomography) and CT (computed tomography)] imaging methods. There are several review articles that provide extensive coverage of the use of these imaging modalities in the context of imaging cardiac ECM [11; 12]. The major limitation with invasive imaging methods is that clinical translation can be limited due to the general use of ex vivo tissue specimens requiring biopsies obtained by specialised surgical procedures and are therefore not readily available. Non-invasive imaging methods overcome this limitation as they provide in vivo imaging which can be applied safely to the patient. This review aims to address the latest developments in the field of non-invasive imaging of ECM changes that are associated with CVD. Whilst we briefly mention other imaging modalities, the scope and focus of this review is on MRI and PET applications. The review also provides a summary of the basic components that comprise the ECM and their biosynthetic pathways that enable a better understanding of the development of targeted probes for imaging of the ECM.