Figure 3.

Illustration of the exosome-mediated cross-talk among cardiomyocytes and other cardiac cell types in the heart, such as fibroblasts, macrophages, and adipocytes, during hypertrophic signaling.Under angiotensin II and pressure overload stresses, exosomes derived from fibroblasts (A) and macrophages (B) containing miR-21* and miR-155, respectively, can downregulate SPRBS2, PDLIM5, and Socs1 and activate several components of angiotensin signaling pathway in cardiomyocytes, eventually resulting in the development of hypertrophy. C: adipocytes could remotely enhance cardiac hypotrophy by mTOR activation-meditated exosomal miR-200a expression in response to rosiglitazone treatment.