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2015 ; 7
(6
): 306-10
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Perspective of future drugs targeting sterile 20/SPS1-related
proline/alanine-rich kinase for blood pressure control
#MMPMID26131334
Lin GM
; Liu PY
; Wu CF
; Wang WB
; Han CL
World J Cardiol
2015[Jun]; 7
(6
): 306-10
PMID26131334
show ga
According to a genome-wide association study, intronic SNPs within the human
sterile 20/SPS1-related proline/alanine-rich kinase (SPAK) gene was linked to 20%
of the general population and may be associated with elevated blood pressure. As
cell volume changes, mammalian SPAK kinases respond to phosphorylate and regulate
cation-coupled chloride co-transporter activity. To our knowledge,
phosphorylation of upstream with-no-lysine (K) (WNK) kinases would activate SPAK
kinases. The activation of WNK-OSR1/SPAK cascade on the kidneys and aortic tissue
is related to the development of hypertension. Several regulators of the WNK
pathway such as the Kelch kinase protein 3 - Cullin 3 E3 ligase,
hyperinsulinemia, and low potassium intake to mediate hypertension have been
identified. In addition, the SPAK kinases may affect the action of
renin-angiotensin-aldosterone system on blood pressure as well. In 2010, two SPAK
knock-in and knock-out mouse models have clarified the pathogenesis of lowering
blood pressure by influencing the receptors on the kidneys and aortic smooth
muscle. More recently, two novel SPAK inhibitors for mice, Stock 1S-14279 and
Closantel were discovered in 2014. Targeting of SPAK seems to be promising for
future antihypertensive therapy. Therefore we raised some viewpoints for the
issue for the antihypertensive therapy on the SPAK (gene or kinase).