Table 2.

Cathepsin activities in CVD.

Cathepsin activity	Cathepsins	Functions relevant to CVD
Inflammation	CatB, CatL	Cytokine/chemokine proteolytic activation [135, 136]
	CatB, CatL	NLRP3 inflammasome activation [137–139]
Immunity	CatB, CatL, CatF	Antigen presentation, CD4+ T-cell activation, Th17 cell differentiation [140–145, 147–149]
	CatS, CatK, CatL	TLR7 activation, Treg activity suppression [150]
Cell migration	CatS	SMC CX3CR1 release and monocyte capture, monocyte/macrophage trans-endothelium migration [36, 47, 116]
	CatC	Neutrophil serine protease activation and migration [37, 154]
Cholesterol metabolism	CatH	LDL modification and foam cell formation [158]
	CatF, CatB, CatK, CatS, CatL, CatV	apoB-100 cleavage, LDL aggregation [99, 159]
	CatS, CatF, CatK, CatB	apoA-1 degradation, cholesterol efflux inhibition [161–163]
Angiogenesis	CatS	PAR-2 activation and endothelium damage, collagen-IV-derived canstatin and arresten degradation, laminin-5 γ2 fragment generation [23, 57, 163]
	CatK	EC proliferation and invasion [60]
	CatL	EPC homing to injured vasculature [166]
Cell death	CatB, CatL, CatS, CatK	Bid proteolysis into tBid and consequent cytochrome C release from the mitochondria [170, 171, 174–177]
Autophagy	CatL, CatS, CatB	Required for HUVEC, HAEC, and macrophage autophagy, but reduce cardiomyocyte autophagic degradation, required for HUVEC, cardiomyocyte, and macrophage survival, but increase HAEC death, required for M2 macrophage polarization [126, 183, 185, 188, 191]
Cell signaling and tissue fibrosis	CatB, CatL	EGF/EGF receptor complex intracellular degradation [192–195]
	CatB, CatX	IGF-1 degradation [196, 197]
	CatS, CatK, CatB, CatL	TGF-β signaling and tissue fibrosis (Figures 2 and 4) [200, 205]