Review Article

Adipose Tissue-Derived Extracellular Vesicles: A Promising Biomarker and Therapeutic Strategy for Metabolic Disorders

Table 1

Role of EVs from adipose tissue and different cells of adipose tissue in metabolic diseases.

SourceInteracting cellsCargosMechanisms and rolesDiseasesReferences

Adipose tissueAdipocyteMitochondria componentsMitigate the syndrome in high-fat-diet miceObesity[19]
AdipocyteNPM3Regulate the stability of PRDM16 mRNA and enhance the expression of browning-related genesObesity[20]
miRNAsImprove glucose tolerance and reduce hepatic FGF21 mRNA and circulating FGF21Obesity[21]

AdipocyteSkeletal muscle cellmiR-27aInduction of insulin resistance in skeletal muscle by inhibition of PPARγT2DM[22]
Hepatocytes, skeletal muscle cellmiR-222Inhibition of insulin receptor-1 expression promotes insulin resistance in liver and skeletal muscle cells of obese miceT2DM[23]
HepatocyteMitochondria-associated proteinsPromotes oxygen consumption in receptor cells, reduces lipid accumulation, and lowers blood glucoseObesity[19]
AdipocyteAdipokineInhibition of insulin-induced AKT phosphorylation impairs insulin signaling in hepatocytesInsulin resistance[24]
Reduced insulin-stimulated glucose uptakeInsulin resistance[25]
CardiomyocytemiR-802-5pTargeting HSP60 promotes insulin resistance in cardiomyocytesCardiovascular diseases[26]
iNOSβ3-Adrenergic receptors in brown adipocytes inhibit iNOS-mediated cardioprotection in EVsCardiovascular diseases[27]
MacrophageRegulation of macrophage foam cell formation and polarization promotes atherosclerosisCardiovascular diseases[28]
LipidsModulate tissue macrophage differentiation and functionObesity[29]
miR-34aInhibition of macrophage M2 polarization promotes obesity-induced adipose inflammationObesity[30]
Pancreatic β-cellInsulinotropic proteinEnhancement of insulinotropic GPCR/cAMP/PKA signaling pathway to enhance insulin releaseInsulin resistance[31]
miRNAsAffects proliferation and function of pancreatic β-cellsObesity[32]
Hypothalamic neuronal cellMALAT1Inhibits miRNA function, affects mTOR signaling, and regulates energy intakeObesity[33]
Colorectal cellsMTTPMTTP/proline-rich acidic protein 1 (PRAP1) complex inhibits the expression of zinc finger E-box-binding homology box 1 and upregulates glutathione peroxidase 4 and xCT, leading to a decrease in polyunsaturated fatty acid ratio and lipid ROS levelsAdvanced colorectal cancer[34]

MacrophageMacrophageModulation of adipose tissue function and insulin sensitivity promotes activation of macrophage M1 proinflammatory phenotypeInsulin resistance[35]
Adipocyte, muscle cellmiR-155Inhibition of target gene PPARγ suppresses insulin signaling and glucose toleranceInsulin resistance[36]
Adipocyte, myocyte, hepatocytemiR-29aModulation of obesity-associated insulin resistanceObesity[37]
AdipocytemiRNAsAffects adipocyte gene expression, differentiation, and insulin-dependent glucose uptakeObesity[38]
MiR-210Targeting NDUFA4 gene expression regulates glucose uptake and mitochondrial CIV activation to promote diabetes progressionT2DM[39]
MacrophagemiR-222-3pModulation of macrophage polarization improves diabetic wound healingDiabetic ulcer[40]
CardiomyocytemiR-140-5pRegulation of glutathione synthesis promotes iron death-induced cardiac injuryCardiovascular diseases[41]

Adipose-derived stem cellsMacrophageTyrosine hydroxylasePolarized M2 macrophages and white adipose tissue aggregates attenuate adipose inflammation and obesityObesity[42]
PodocyteEnhanced miR-486 expression improves diabetic nephropathyT2DM[43]
FibroblastmiRNAActivation of PI3K/Akt signaling pathway promotes diabetic wound healing and inhibits inflammatory responseDiabetic ulcer[44]
Vascular endothelial cellGlyoxalase 1Activation of eNOS/AKT/ERK/P-38 signaling pathway, inhibition of AP-1/ROS/NLRP3/ASC/Caspase-1/IL-1β, and release of VEGF, IGF-1, and FGF to promote angiogenesisT2DM[45]

Endothelial cellsAdipocyteCav1Endothelial cells transport Cav1-containing EVs to adipocytes to form Cav1-containing adipocyte EVsObesity[46]