Abstract
Fibrosis is a significant global health problem associated with many inflammatory and degenerative diseases affecting multiple organs, individually or simultaneously. Fibrosis develops when extracellular matrix (ECM) remodeling becomes excessive or uncontrolled and is associated with nearly all forms of heart disease. Cardiac fibroblasts and myofibroblasts are the main effectors of ECM deposition and scar formation. The heart is a complex multicellular organ, where the various resident cell types communicate between themselves and with cells of the blood and immune systems. Exosomes, which are small extracellular vesicles, (EVs), contribute to cell-to-cell communication and their pathophysiological relevance and therapeutic potential is emerging. Here, we will critically review the role of endogenous exosomes as possible fibrosis mediators and discuss the possibility of using stem cell-derived and/or engineered exosomes as anti-fibrotic agents.
Highlights
As a result of this study, it was found that miRNAs, Long non-coding RNAs (lncRNAs), and mRNAs are loaded in a selective manner and that these molecules can be transferred from cell to cell via exosomes
In order for exosome-based therapies to become realistic candidates for adoption as the treatment of cardiac fibrosis in the clinical practice, we propose that they should satisfy at least some of the following six aspirations, being able to (i) limit fibrosis through reduction of collagen deposition in the myocardium and/or inhibition of pro-fibrotic factors; (ii) reduce formation of myofibroblasts in the heart; (iii) be cardioprotective, i.e., reduce apoptosis of CMs and other cell types; (iv) promote blood flow recovery by increasing microvascular density; (v) selectively target cells involved in the disease with a therapeutic molecular cargo personalized to each cell type; (vi) improve cardiac function
It was identified that mesenchymal stem cells (MSCs) and exosomes collected from them have a similar expression pattern of miRNAs. miRNAs involved in cardiac fibrosis were described in the work of Shao et al and discussed in the miRNAs chapter [108]
Summary
Fibrosis is a well-recognized cause of morbidity and mortality. Fibrotic diseases cause more than. Cells 2020, 9, 592 two types of cardiac fibrosis, which are the most relevant for the remodeling of the ischemic adult heart: (1) reactive interstitial fibrosis is characterized by an increase in collagen synthesis and diffused deposition of collagen that leads to an increased interstitial compartment volume without loss of myocytes. This type of fibrosis occurs progressively in response to increased pressure and/or volume loads as in the cases of hypertension, aortic stenosis, ageing, and diabetes. In replacement fibrosis, which is currently not reversible, the affected myocardium is not viable and unable to recover contractile properties
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