Adipose tissue‑derived extracellular vesicles: Systemic messengers in health and disease (Review)

Figures

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  Figure 1.. EV biogenesis, release, and communication with recipient cells. Exosomes and MVs released from cells are primarily stratified based on size. In addition, MVs can bud from the plasma membrane, while exosomes are derived from ILVs within the lumen of MVBs. MVBs then fuse with the plasma membrane to release the exosomes. EVs transport nucleic acids, proteins, and lipids to target cells by (1) membrane fusion, (2) endocytosis, and (3) ligand binding mechanisms to exert their biological functions. EV, extracellular vesicle; MVs, microvesicles; ILVs, intraluminal vesicles; MVBs, multivesicular bodies.

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  Figure 2.. ADEV-mediated crosstalk between ATs and other organs. ATs secrete EVs containing various components into the blood circulation to affect ATs and distant organs. In ATs and the liver, miRNAs contained in ADEVs result in insulin resistance by inhibiting the activation or expression of PPARα, PPARγ, PPARδ, or IRS-1. In the brain, ADEVs contain lncRNA MALAT1, which enhances mTOR signaling in POMC neurons, leading to increased appetite and a gain in body gain. miR-200a contained in ADEVs can be delivered to cardiomyocytes to inhibit TSC1 and activate the mTOR pathway, leading to cardiac hypertrophy. ATs, adipose tissues; ADEVs, AT-derived extracellular vesicles; WAT, white AT; BAT, brown AT; miR, microRNA; lnc, long non-coding RNA; TSC1, tuberous sclerosis complex 1; PPAR, peroxisome proliferator-activated receptor; IRS-1, insulin receptor substrate 1; MALAT1, metastasis-associated lung adenocarcinoma transcript 1.