The role of exosomes and exosomal microRNA in diabetic cardiomyopathy

Figures

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  Figure 1. Exosome biogenesis. Cell membrane invagination initiates the formation of early inner nuclear bodies (A). Various buds enter the endosomal lumen, commencing the generation of exosomes/intracavitary vesicles (B) within late sorting endosomes. Cargo molecules are translocated between the trans-Golgi network (C), endoplasmic reticulum (D), and the late sorting endosome (B). Collectively, these processes culminate in the creation of multivesicular bodies (E) that contain fully developed luminal vesicles/exosomes. Multivesicular bodies can subsequently undergo intracellular processing via lysosomes (F) or autophagosomes (G), resulting in the breakdown of the multivesicular body’s components within the cell. Alternatively, these polyvesicles can dock (H) and fuse with the cell membrane, releasing exosomes (I) into the extracellular space. Exosomes consistently express various surface markers (J) that can be used for characterization. The functions of exosomes (K) are contingent on the diverse cargoes they encapsulate within the exobody.

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  Figure 2. Signaling pathways are regulated by miRNA in diabetic cardiomyopathy. (A) The expression of miR-34a in H9c2 of rat cardiomyocytes treated with high glucose was up-regulated, the expression of miR-34a-targeted anti-apoptosis protein (Bcl-2) decreased, and the apoptosis rate of H9c2 cells increased. Overexpression of miR-195 can down-regulate the expression of Bcl-2,miR-195, reduce the production of ROS and inhibit apoptosis. miR-1 was up-regulated, and the activity of pro-apoptotic factor caspase-3 was increased. (B) MiR-30c and miR-181a cooperatively regulate p53-p21 pathway, improve cardiac structure and function, and pathological hypertrophy in diabetes-induced cardiac hypertrophy.MiR-1 delays the process of cardiomyocyte hypertrophy by negatively regulating calcium signal components calmodulin, cardiac transcriptional regulatory factor (GATA4) and cardiomyocyte enhancer factor 2A (MEF2A). (C) MiRNA inhibits angiogenesis by inhibiting the proliferation and migration of vascular endothelial cells,it can also promote angiogenesis. (D) Some miRNA can inhibit myocardial fibrosis through related pathways and proteases.