Abstract
Cardiovascular diseases (CVDs) represent a major global health problem, due to their continued high incidences and mortality. The last few decades have witnessed new advances in clinical research which led to increased survival and recovery in CVD patients. Nevertheless, elusive and multifactorial pathophysiological mechanisms of CVD development perplexed researchers in identifying efficacious therapeutic interventions. Search for novel and effective strategies for diagnosis, prevention, and intervention for CVD has shifted research focus on extracellular vesicles (EVs) in recent years. By transporting molecular cargo from donor to recipient cells, EVs modulate gene expression and influence the phenotype of recipient cells, thus EVs prove to be an imperative component of intercellular signaling. Elucidation of the role of EVs in intercellular communications under physiological conditions implied the enormous potential of EVs in monitoring and treatment of CVD. The EVs secreted from the myriad of cells in the cardiovascular system such as cardiomyocytes, cardiac fibroblasts, cardiac progenitor cells, endothelial cells, inflammatory cells may facilitate the communication in physiological and pathological conditions. Understanding EVs-mediated cellular communication may delineate the mechanism of origin and progression of cardiovascular diseases. The current review summarizes exosome-mediated paracrine signaling leading to cardiovascular disease. The mechanistic role of exosomes in cardiovascular disease will provide novel avenues in designing diagnosis and therapeutic interventions.
Highlights
Described initially as debris with no functional significance or potential involvement in the clearance of damaged cellular components, extracellular vesicles (EVs) represent a heterogenous population of vesicles
In the study investigating delivery free fatty acids (FFAs) from the bloodstream to cardiac tissue, the results demonstrated the exosome-mediated mechanism of circulating FFAs delivery from blood to tissue
Molecular cargo transferred by exosomes modulates cardiac homeostasis in physiological conditions
Summary
Described initially as debris with no functional significance or potential involvement in the clearance of damaged cellular components, extracellular vesicles (EVs) represent a heterogenous population of vesicles. KLF5-overexpressing VSMCs exerted pro-atherosclerotic effect by secretion of miR-155 enriched exosomes Uptake of these exosomes by ECs resulted in inhibition of cell proliferation and migration and disrupted endothelial barrier integrity. The activation of CD137 inflammatory signaling in endothelial cells (ECs) downregulates TET2 expression in EC-derived exosomes This CD137 signaling-mediated exosomal downregulation of TET2 expression resulted in a pro-proliferation, phenotype switch of VSMCs, and intimal hyperplasia after arterial injury. The atherogenic effects of miR-1 were attributed due to the downregulation of KLF4 and NF-kB pathway activation in ECs. Inhibition of miR-1 attenuated endothelial inflammation and atherogenesis suggesting the role of hepatocyte-derived exosomes in the pathogenesis of vascular complication [51]. An in-vitro study reported the role of exosome-mediated lncRNA ZEB1-AS1 and its underlying mechanisms in atherogenesis in HUVECs. In ox-LDL-stimulated HUVECs, exosomal lncRNA ZEB1-AS1 facilitates cell injury by miR-590-5p/ETS1 Axis through the TGF-β/Smad Pathway [60]. These studies provide key evidences, understanding the role of exosomal lipid transport in the onset and progression of CVD is extremely limited and warrants further investigations
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