Table 1.

Clinical Use of Metabolomics of EVs in Diagnosis and Therapy

Scheme	Diseases	Source of EVs	Metabolites Studied	Ref.
Diagnosis	Late myocardial necrosis of atherosclerotic	Adipose tissue	C16:0 ceramide and their derivatives	[87]
	Acute pancreatitis	Plasma	Eicosatrienoic acid (C20:3), thiamine triphosphate. 2-Acetylfuran, cis-Citral	[68]
	Gestational hypertension	Plasma	SM, acetyl CoA, methionine, phenylalanine, tryptophan, carotenoids, tyrosine, arginine, leucine	[88]
	ST elevation myocardial infarction	Plasma	Ceramides, dihydroceramides, and sphingomyelins	[69]
	Lung cancer	Pleural effusions	Phenylalanine, leucine, PC 35:0 and SM 44:3	[91]
		Serum	Ceramides, PC and polyunsaturated acyl chains	[92]
	Prostate cancer	Urinary	PS 18:1/18:1 and lactosylceramide (d18:1/16:0)	[93]
	Benign prostate hyperplasia	Urinary	PC, PE, SM	[31]
	Bipolar disorder	Serum	lysoPE 18: 0, lysoPE 14: 0, lysoPC 18: 0, and lysoPC 20: 1	[73]
	Schizophrenia
	Depressive disorder
	Chromochromic leukogystrophy	Brain tissue	sulfides of short fatty acyl chains	[82]
	Multiple sclerosis	Plasma	C16:0 sulfatide	[98]
Therapy	Drug- and noise-related hearing loss	Auditory cells	Eicosanoids	[104]
	Advanced Alzheimer’s disease	Microglia	Cholesterol, docosahexaenoic acid (DHA)	[83]

Abbreviations: PE, phosphatidylethanolamine; PI, phosphatidylinositol; PC, phosphatidylcholine; PS, phosphatidylserine; PA, phosphatidic acid; SM, sphingomyelins.