Literature summary for 3.4.21.118 extracted from

Cao, B.; Yu, Q.; Zhao, W.; Tang, Z.; Cong, B.; Du, J.; Lu, J.; Zhu, X.; Ni, X.
Kallikrein-related peptidase 8 is expressed in myocardium and induces cardiac hypertrophy (2016), Sci. Rep., 7, 20024 .

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Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	O88780	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
cardiomyocyte	primary cardiomyocyte	Rattus norvegicus	-
myocardium	KLK8 expression is upregulated in left ventricle of cardiac hypertrophy models	Rattus norvegicus	-

General Information

General Information	Comment	Organism
physiological function	both intra-cardiac adenovirus-mediated and transgenic-mediated KLK8 overexpression leads to cardiac hypertrophy in vivo. In primary neonatal rat cardiomyocytes, KLK8 knockdown inhibits phenylephrine-induced cardiomyocyte hypertrophy, whereas KLK8 overexpression promotes cardiomyocyte hypertrophy via a serine protease activity-dependent but kinin receptor-independent pathway. KLK8 overexpression increases epidermal growth factor production, which is blocked by the inhibitors of serine protease. EGF receptor antagonist and EGFR knockdown reverse the hypertrophy induced by KLK8 overexpression. KLK8-induced cardiomyocyte hypertrophy is also significantly decreased by blocking the protease-activated receptor PAR1 or PAR2 pathway	Rattus norvegicus

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Release 2023.1 (January 2023)