2016
DOI: 10.1111/apha.12758
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c‐Jun N‐terminal Kinase mediates prostaglandin‐induced sympathoexcitation in rats with chronic heart failure by reducing GAD1 and GABRA1 expression

Abstract: Prostaglandin signalling through upregulated PTGER3 activates JNK which reduces GAD1 and GABRA1 expression in the PVN, and contributes to sympathoexcitation in CHF.

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Cited by 4 publications
(2 citation statements)
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References 42 publications
(60 reference statements)
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“…The non-selective EP receptor antagonist AH6809 has been widely applied to explore the roles of PGE2/EP2 signaling under normal and pathological conditions (109). Although AH6809 acts as an antagonist of EP2, it may also serve as an antagonist of EP1 and dP1 (110); it is neither selective nor potent, and is therefore unsuitable for in vivo studies (111).…”
Section: Development Of Agonists Antagonists and Targeted Drugs For Ep2mentioning
confidence: 99%
“…The non-selective EP receptor antagonist AH6809 has been widely applied to explore the roles of PGE2/EP2 signaling under normal and pathological conditions (109). Although AH6809 acts as an antagonist of EP2, it may also serve as an antagonist of EP1 and dP1 (110); it is neither selective nor potent, and is therefore unsuitable for in vivo studies (111).…”
Section: Development Of Agonists Antagonists and Targeted Drugs For Ep2mentioning
confidence: 99%
“…The mechanisms causing the increase in renal sympathetic nerve activity remain to be elucidated. Wang et al have recently described how c‐Jun N‐terminal Kinase reduces GAD1 and GABRA1 expression, thereby mediating prostaglandin‐induced sympatho‐excitation in a rat model of chronic heart failure. Lu et al describe that renal denervation benefits cardiac angiogenesis during sustained pressure overload by a regulation of VEGF and VEGFR2 expression and eNOS activation.…”
Section: Contractile Function and Heart Failurementioning
confidence: 99%