Discovered in the late 1980s as an extracellular vesicle of endosomal origin secreted from reticulocytes, exosomes recently gained scientific attention due to its role in intercellular communication. Exosomes have now been identified to carry cell-specific cargo of nucleic acids, proteins, lipids, and other biologically active molecules. Exosomes can be selectively taken up by neighboring or distant cells, which has shown to result in structural and functional responses in the recipient cells. Recent advances indicate the regulation of exosomes at various steps, including their biogenesis, selection of their cargo, as well as cell-specific uptake. This review will shed light on the differences between the type of extracellular vesicles. In this review, we discuss the recent progress in our understanding of the regulation of exosome biogenesis, secretion, and uptake.

https://link.springer.com/content/pdf/10.1007/s11010-020-03703-z.pdf

Inside(sight) of tiny communicator: exosome biogenesis, secretion, and uptake

Long known as digestive organelles, lysosomes have now emerged as multifaceted centers responsible for degradation, nutrient sensing, and immunity. Growing evidence also implicates role of lysosome-related mechanisms in pathologic process. In this review, we discuss physiological function of lysosomes and, more importantly, how the homeostasis of lysosomes is disrupted in several diseases, including atherosclerosis, neurodegenerative diseases, autoimmune disorders, pancreatitis, lysosomal storage disorders, and malignant tumors. In atherosclerosis and Gaucher disease, dysfunction of lysosomes changes cytokine secretion from macrophages, partially through inflammasome activation. In neurodegenerative diseases, defect autophagy facilitates accumulation of toxic protein and dysfunctional organelles leading to neuron death. Lysosomal dysfunction has been demonstrated in pathology of pancreatitis. Abnormal autophagy activation or inhibition has been revealed in autoimmune disorders. In tumor microenvironment, malignant phenotypes, including tumorigenesis, growth regulation, invasion, drug resistance, and radiotherapy resistance, of tumor cells and behaviors of tumor-associated macrophages, fibroblasts, dendritic cells, and T cells are also mediated by lysosomes. Based on these findings, a series of therapeutic methods targeting lysosomal proteins and processes have been developed from bench to bedside. In a word, present researches corroborate lysosomes to be pivotal organelles for understanding pathology of atherosclerosis, neurodegenerative diseases, autoimmune disorders, pancreatitis, and lysosomal storage disorders, and malignant tumors and developing novel therapeutic strategies.

/pdf/role-of-lysosomes-in-physiological-activities-diseases-and-2jq8pjz6nd.pdf

Role of lysosomes in physiological activities, diseases, and therapy

Exosomes are nanosized lipid vesicles originating from the endosomal system that carry many macromolecules from their parental cells and play important roles in intercellular communication. The functions and underlying mechanisms of exosomes in atherosclerosis have recently been intensively studied. In this review, we briefly introduce exosome biology and then focus on advances in the roles of exosomes in atherosclerosis, specifically exosomal changes associated with atherosclerosis, their cellular origins and potential functional cargos, and their detailed impacts on recipient cells. We also discuss the potential of exosomes as biomarkers and drug carriers for managing atherosclerosis.

Exosomes in atherosclerosis: performers, bystanders, biomarkers, and therapeutic targets.

Cardiac exosomes mediate cell-to-cell communication, stimulate or inhibit the activities of target cells, and affect myocardial hypertrophy, injury and infarction, ventricular remodeling, angiogenesis, and atherosclerosis. The exosomes that are released in the heart from cardiomyocytes, vascular cells, fibroblasts, and resident stem cells are hypoimmunogenic, are physiologically more stable than cardiac cells, can circulate in the body, and are able to cross the blood-brain barrier. Exosomes utilize three mechanisms for cellular communication: (1) internalization by cells, (2) direct fusion to the cell membrane, and (3) receptor-ligand interactions. Cardiac exosomes transmit proteins, mRNA, and microRNAs to other cells during both physiological and pathological process. Cardiac-specific exosome miRNAs can regulate the expression of sarcomeric genes, ion channel genes, autophagy, anti-apoptotic and anti-fibrotic activity, and angiogenesis. This review discusses the role of exosomes and microRNAs in normal myocardium, myocardial injury and infarction, atherosclerosis, and the importance of circulating microRNAs as biomarkers of cardiac disease. Graphical Abstract.

Cardiovascular Exosomes and MicroRNAs in Cardiovascular Physiology and Pathophysiology

Background Tumor microenvironment (e.g., cancer-associated fibroblast) plays a key role in cancer tumorigenesis and metastasis. However, the detailed mechanism of whether hypoxia promotes CRC progression via tumor microenvironment remains unclear. Methods In this study, circEIF3K exosome was examined by NanoSight Tracking Analysis and RT-qPCR. We used cell colony formation assay, transwell assay and tube formation assay to determine proliferation, invasion and metastasis of HCT116 or SW620 cells. Xenograft tumor assay was employed to show in vivo tumor growth of HCT116 cells. Results We found that hypoxia could induce secretion of circEIF3K exosome. Conditioned medium (CM) and exosome from circEIF3K knockdown CAF significantly attenuated proliferation, invasion and tube formation of HCT116 or SW620 cells, which could be reverted by miR-214 under hypoxia treatment. Besides, we observed that circEIF3K knockdown evidently impaired tumor growth in mice. TCGA dataset analysis showed that low expression of circEIF3K was observed in normal tissues and associated with prolonged survival time. Finally, PD-L1 was confirmed as important target for miR-214 in CRC. Conclusion In conclusion, our study reveals that a novel axis circEIF3K/miR-214/PD-L1 mediates hypoxia-induced CRC progression via CAF, providing the rationale for developing new targeted therapeutics to treat CRC.

/pdf/exosomal-circeif3k-from-cancer-associated-fibroblast-430crbulve.pdf

Exosomal circEIF3K from cancer-associated fibroblast promotes colorectal cancer (CRC) progression via miR-214/PD-L1 axis.

Exosomes: An emerging factor in atherosclerosis

Corrigendum to "Exosomes: An emerging factor in atherosclerosis" [Biomed. Pharmacother. 115 (2019) 108951].

Bushen Kangshuai tablet inhibits progression of atherosclerosis by intervening in macrophage autophagy and polarization.

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Exosomes: An emerging factor in atherosclerosis

Corrigendum to "Exosomes: An emerging factor in atherosclerosis" [Biomed. Pharmacother. 115 (2019) 108951].

Bushen Kangshuai tablet inhibits progression of atherosclerosis by intervening in macrophage autophagy and polarization.