Table 2.

Potential proteomic biomarkers in keloids

Biomarker	Abbreviation	Involved physiological function	Expression in keloids	Associated biological processes in keloids	Role in keloids	Reference
Forkhead Box F2	FOXF2	Cell proliferation Cell invasion	Up-regulated	Maintenance of extracellular matrix-related gene expression	Involvement in the pathogenesis of keloids Potential therapeutic target	[114]
Hypoxia inducible factor 1 subunit alpha	HIF-1α	Energy metabolism Angiogenesis	Up-regulated	Metabolic adaptation to hypoxia	Involvement in the pathogenesis of keloids	[93, 120]
Heat shock protein 70	HSP70	Correct folding of proteins	Up-regulated	HSP70 knockdown decreases collagen production in KFB	Potential therapeutic target	[76, 115]
Heat shock protein 90	HSP90	Cell cycle control Signal transduction	Up-regulated	Regulation of apoptosis, proliferation and migration of fibroblasts Heat shock protein 90 inhibitor induces apoptosis and reduces cell migration in keloid fibroblasts	Potential therapeutic target	[116]
High-temperature requirement A serine peptidase 1	HTRA1	Cell growth	Up-regulated	Acceleration of cell proliferation Remodeling of keloid-specific ECM	Involvement in the pathogenesis of keloids	[56]
Matrix metalloproteinase 1	MMP-1	Breakdown of ECM	Up-regulated	Regulation of fibroblast migration Regulation of matrix metalloproteinase function	Involvement in the pathogenesis of keloids	[68]
Syndecan-1	SDC1	Cell binding Cell signaling Cytoskeletal organization	Up-regulated	Matrix synthesis	Potential molecular diagnostic biomarker	[111, 113]
Transforming growth factor β-1	TGF-β1	Cell growth Cell differentiation	Up-regulated	Collagen synthesis Fibroproliferation	Involvement in the pathogenesis of keloids	[38, 71]
TNF-α-stimulated Gene-6	TSG-6	ECM stability Cell migration	Down-regulated	Induction of apoptosis in KFB Remodeling of the extracellular matrix Inflammation	Potential therapeutic target	[117–119]

KFB keloid fibroblast cells, EMT endothelial–mesenchymal transition, ECM extracellular matrix