TABLE 1.

Role of CatK in bone.

Tissues	Diseases	Functions	References
Bone	Pycnodysostosis	Pycnodysostosis-related mutant CatK proteins were incapable of degrading type I collagen. All the CatK mutations identified in Pycno patients were loss-of-function mutations that appeared to eliminate its enzymatic activity.	Gelb et al., 1996; Hou et al., 1999; Nishi et al., 1999
	Postmenopausal osteoporosis	The serum CatK levels were significantly elevated in women with postmenopausal osteoporosis, while they were reduced after the patients were treated with bisphosphonates, the established anti-resorptive agents.	Meier et al., 2006
	OA	The increased expression and collagenase activity of CatK could contribute to the cartilage matrix degradation in OA progression. CatK is currently among the promising therapeutic target candidates for the development of disease-modifying osteoarthritic drugs.	Konttinen et al., 2002; Dejica et al., 2012; Kozawa et al., 2016
	RA	The serum CatK levels were increased in patients with active longstanding RA, which were significantly correlated with the severity of joint destruction. CatK deficiency largely prevented the cartilage erosion and bone destruction and reduced the joint inflammation in mice with TNF-α-mediated arthritis. Inhibition of CatK could suppress the cartilage degradation as well as the systemic and local bone loss to prevent joint destruction in preclinical RA models.	Skoumal et al., 2005; Asagiri et al., 2008; Svelander et al., 2009; Hao et al., 2015; Yamashita et al., 2018; Yamada et al., 2019