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- Thus, cardiac fibrosis is a complex process involving multiple cells and regulated by multiple molecular pathways.
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- It is indeed possible that miR-29b targets a sequence within the TGF-β1 coding area, which explains this observation.
- Exosomes, ranging in 30–150 nm of size, play an essential role in cellular communications by their bioactive contents .
- Another research indicated that miR-27a-, miR-28a-, miR-34a-enriched fibroblast-derived exosomes could regulate cardiomyocyte antioxidant enzymes, thus contributing to cardiac hypertrophy .
In order to clarify the role of CFs and myofibroblasts in cardiac fibrosis, several markers have been found to identify and distinguish CFs and myofibroblasts (13–37) . It has been clear that most CFs derived from the epicardium, a protective epithelial layer that entirely covers the four cardiac chambers, undergoing epithelial–mesenchymal transition . Smaller populations are derived from the endocardium and cardiac neural crest and are mostly found in the interventricular septum and right atrium, respectively . However, the origin of the myofibroblasts forming fibrotic lesions in failing hearts has been a source of debate. Cell therapy, including different types of stem cells, has been widely considered as a therapeutic approach for the treatment of cardiac fibrosis.
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According to increasing evidence, macrophages and monocytes have both been confirmed to play vital roles in the regulation of cardiac fibrosis. Moreover, circulating fibroblast progenitors may be implicated in the progression of cardiac fibrosis as suggested by numerous studies using bone marrow transplantation techniques . These hematopoietic progenitors could be monocyte subsets that can differentiate fibroblasts, comparable with the CD14+ “fibrocytes” discovered in humans , which imply that macrophages and monocytes in fibrotic hearts could be sources of myofibroblasts. Exosome-mediated intercellular signaling, which can transfer various functional modulators including proteins, lipids, and RNA, plays an increasingly important role in cardiovascular diseases.
On the contrary, anti-fibrotic mediators could also be produced by endothelial cells. Endothelial cells have been found to express hypoxia-inducible factor -1 for protecting the pressure-overloaded myocardium from fibrosis via suppression of TGF-β signaling partially . Furthermore, endothelial cells exert inhibitory actions on cardiac fibrosis by producing and secreting interferon-γ-inducible protein -10/CXCL10, a CXC chemokine that prevents the migration of CFs in the infarcted heart . In response to different physiological states, exosomes are secreted by various cell types, such as MCs , macrophages, CFs, and exogenous MSCs, whose size range from 30 to 150 nm. Initially, transmembrane proteins are endocytosed and trafficked to early endosomes . EEs then mature into late endosomes and generate intraluminal vesicles in the lumen of the organelles.
It is indeed possible that miR-29b targets a sequence within the TGF-β1 coding area, which explains this observation. On the contrary, AT2 signaling may inhibit AT1-mediated actions, suppressing CF proliferation and matrix synthesis, serving as a negative regulator of Ang II-mediated profibrotic responses. Exosomes, ranging in 30–150 nm of size, play an essential role in cellular communications by their bioactive contents . As a cell-free system, exosomes could lead to improvement in cardiac function without triggering an immune response by including cardioprotective components such as miRNAs and proteins, emerging as an appropriate candidate for cardiac fibrosis treatment. Recent research studies show that inhibiting exosome secretion or targeting specific molecules in CF-derived exosomes could be a promising therapeutic strategy in ischemic heart disease . In this review, we demonstrate the current understandings of the cellular effectors, molecular pathways, and exosomal roles in cardiac fibrosis.
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MCGs are known to contain TGF-β in a large amount, while TGF-β-induced Smad-dependent pathways are activated by MC chymase, which results in fibrogenic effects . Besides, profibrotic growth factors including TGF-β can be produced and secreted in significant quantities by macrophages and monocytes. In return, TGF-β-mediated actions of these cell types may also play a paracrine role in fibrotic response. Moreover, endothelial cells may promote fibrotic cardiac remodeling through the expression of profibrotic mediators, such as TGF-β1, FGFs, or ET-1.
First, aldosterone may have pro-inflammatory effects on vascular cells by increasing the production of cytokines like TNF-α via NF-κB activation. Second, aldosterone may induce a fibrogenic phenotype in macrophages via the mineralocorticoid receptor. Third, aldosterone may activate cardiomyocyte-derived fibrotic signals, involving regulation of MMP-2/9 activity and the TGF-β-connective tissue growth factor profibrotic pathway. Fourth, aldosterone may exert a direct effect on CFs, stimulating proliferation and increasing collagen synthesis.
- Moreover, endothelin antagonists are now approved to treat pulmonary hypertension, and many believe they will also be beneficial in the treatment of heart pathological fibrosis.
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- Therefore, it is essential to discover potential diagnostic or therapeutic targets for cardiac fibrosis.
- The ETA and ETB receptors, which have been found to perform opposite roles, are two recognized ET-1 receptors in the heart.
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CFs are major components of the heart, ischemia/hypertrophy activates these fibroblasts, and they are involved in cardiac fibrosis and remodeling . Post-cardiac injury, fibroblast-derived miR-21-enriched exosomes can lead to cardiac myocyte hypertrophy and remodeling . In addition, miR-155 enriched in macrophage-derived exosomes led to enhanced proliferation and differentiation of resident fibroblasts and further exacerbated inflammation .
Click calculate to see the size of your profit in both fiat currency and the cryptocurrency of your choice. WJ and YX determined the topic, wrote the initial draft, and revised the manuscript according to the reviewers’ comments. XL searched the related literatures and supplemented the content of the manuscript. YY supervised the planning and execution of the research activity. All authors have given approval to the final version of the manuscript, responsible for the accuracy, and authenticity of the article. After teaching financial english for government departments and commercial banks throughout Asia, Jonathan had a front row seat to the slow motion demise of the current economic model.
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It is widely known that cardiac fibrosis can provoke chamber dilation, cardiomyocyte hypertrophy, and apoptosis and finally result in congestive heart failure (6–8). Therefore, it is essential to discover potential diagnostic or therapeutic targets for cardiac fibrosis. It has been reported that activation of adrenergic signaling via β-adrenergic receptor can induce cardiomyocyte death and subsequent reparative fibrosis, thus leading to cardiac remodeling. Although there are several subtypes of β-AR expressed in the heart, the predominant form of β2-AR seems to be expressed on CFs. Collagen secretion, cell proliferation, migration, and transformation to the myofibroblast phenotype can all be induced by direct activation of β2-AR on CFs, mediated through p38 MAPK signaling partially. In addition, β-AR signaling can also regulate cytokine expression by macrophages and induce growth factor synthesis by cardiomyocytes, which plays an important role in promoting cardiac fibrosis.
The roles of cardiomyocytes in the process of cardiac fibrosis are two sides of the coin. For one thing, cardiomyocytes may promote interstitial fibrosis through neurohumoral and growth factor-mediated pathways, such as cardiomyocyte-specific mineralocorticoid receptor signaling , TGF-β receptor II (TβRII) signaling , and insulin-like growth factor -1 signaling . Moreover, necrotic cardiomyocytes trigger an inflammatory response that finally leads to activation of fibroblasts via release of DAMPs, which means cardiac fibrosis may occur due to cardiomyocyte death, instead of cardiomyocyte-derived fibrogenic signals . For another, cardiomyocyte-specific overexpression of angiotensin II type 2 receptor or the plasminogen activator inhibitor -1 exerts anti-fibrotic actions via the kinin/NO system activation or inhibition of TGF-β synthesis, respectively . After a myocardial injury, CFs convert to their activated form by upregulating expression of pro-inflammatory cytokines, which is defined as the key cellular event in cardiac fibrosis. In addition, TGF-β is a critical fibrogenic mediator that may have the potential to affect all cell types involved in cardiac fibrotic response.
The prevalence of perivascular fibrosis in the injured heart may indicate that endothelial cells are involved in cardiac fibrosis . Under pathophysiologic conditions, endothelial cells may enhance fibrotic responses via a variety of mechanisms after the myocardial injury. First, several profibrotic mediators produced by endothelial cells, such as FGFs, TGF-1, and endothelin -1, may play key roles in the development of cardiac fibrosis .
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According to the location of cardiac scars and underlying cause , cardiac fibrosis can be classified into various forms, among which reactive interstitial fibrosis and replacement fibrosis are the most relevant type of the ischemic adult heart. Being the major cell type in the adult myocardium, CFs perform a critical role in maintaining ECM protein homeostasis. The activation of CFs can lead to the transition into myofibroblasts, which is a critical step in the development of cardiac fibrosis. Besides CFs, there are various types of cells involved in the process of cardiac fibrosis via different pathways.
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Second, endothelial cells may produce pro-inflammatory cytokines and chemokines, contributing to recruitment of lymphocytes and macrophages with fibrogenic actions . Third, although low numbers of endothelial-derived fibroblasts were detected in the remodeling myocardium, endothelial cells may undergo endothelial to mesenchymal transition , increasing the number of fibroblasts . MCs, on the other hand, secrete anti-inflammatory mediators including IL-10 , which has been shown to inhibit excessive cardiac remodeling by activating STAT3 and suppressing NF-κB (56–58). Besides, MCs can produce vascular endothelial growth factor -A , as one of the important anti-fibrotic mediators, which can increase capillary density in damaged tissues and promote proper repair in cardiac fibrosis (59–61). Over the past few years, various studies have been carried out for investigating the functions of MCG in fibrosis.
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