Molecular Advances in Myocardial Fibrosis

Dear Colleagues,

Myocardial fibrosis (MF) is a pathological remodelling process defined by the excessive accumulation in the myocardium of extracellular matrix components, produced by cardiac fibroblasts. This process is the common final pathway of several ischemic and non-ischemic conditions promoting cardiac fibrosis, such as hypertensive, diabetic and idiopathic cardiomyopathy. MF progression is associated with higher morbidity and mortality. Currently, there are a number of invasive and non-invasive modalities for MF assessment. The “gold standard” for quantification of collagen deposition and diagnosing diffuse MF is endomyocardial biopsy (EMB), which is limited, however, by the potential risks associated with its invasive nature. Beyond EMB, MF may be identified through a number of non-invasive techniques, such as cardiac magnetic resonance imaging (CMRI), which defines tissue characteristics through direct observation of the changes in the acquired myocardial tissue images. Unlike EMB and CMRI, serum biomarkers of MF, such as C-terminal telopeptide of collagen 1 (CITP), matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), transforming growth factor β(TGF-β), procollagen type 1 N-terminal propeptide (PINP), galectin-3, osteopontin and soluble interleukin 1 receptorlike 1 (sST2), seem to be more advantageous for diagnosis, therapeutic monitoring and prognosis. However, they should be considered mostly experimental, with variable sensitivity and specificity in different settings, and absolutely not widely implemented in clinical practice.

Recent evidence has highlighted the emerging role of short non-coding RNA molecules, called microRNAs, in governing fibroblast activation and/or contributing to fibrotic remodelling. Nevertheless, the lack of inter- and intra-laboratory standardization make them “putative biomarkers” and a prerogative of research. In the last few years, a number of authors have employed two-dimensional speckle tracking echocardiography for evaluating the impact of MF on cardiac kinetics and function. A strong inverse correlation between the degree of MF and the magnitude of myocardial strain parameters has been demonstrated in various clinical settings. Importantly, MF has been proposed to play an important pathogenetic role in ventricular dysfunction in obesity. A wide range of pathophysiologic conditions, such as volume and pressure overload, hyperglycaemia, insulin resistance and metabolic dysfunction and systemic inflammation, may trigger MF in individuals with obesity. However, their relative role in mediating MF is poorly defined. Activation of fibroblasts likely plays a major role in obesity-associated fibrosis; however, inflammatory cells, cardiomyocytes and vascular cells may also contribute to fibrogenic signalling. In addition, several molecular processes and miRNAs may play a role in the development of obesity and related metabolic complications.

The goal of this Special Issue is to further expand our knowledge of the molecular and pathophysiological mechanisms of myocardial fibrosis in individuals with obesity, as well as to offer a complete and broad view of the current situation in the area, and its future projection, pointing out the new indications that will enrich this field. In this Special Issue, we welcome innovative and original research articles, as well as high-quality review articles with pioneering opinions with a focus on the molecular, clinical and instrumental evaluation of cardiac fibrosis in individuals with obesity.

Dr. Andrea Sonaglioni
Guest Editor

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• obesity
• myocardial fibrosis
• subclinical myocardial dysfunction
• fibrotic remodelling
• microRNAs