New Therapeutic Targets in Cardiology

Rokita, Adam G.; Anderson, Mark E.

doi:10.1161/circulationaha.112.124990

Cited by 98 publications

(65 citation statements)

References 127 publications

(170 reference statements)

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“…The reports of CaMKII-catalyzed hyperphosphorylation have suggested the therapeutic use of CaMKII inhibitors in AF (13,30); however, our evidence indicates that CaMKII-dependent phosphorylation is either reduced or unchanged in human AF. Phosphorylation of PLB at Thr-17 in trabeculae in the operating theater (SI Appendix, Fig.…”

Section: Kn-93 Reduces Ne-evoked Increases Of I Cal In Patients Withcontrasting

confidence: 54%

Arrhythmias, elicited by catecholamines and serotonin, vanish in human chronic atrial fibrillation

Christ

Rozmaritsa²,

Engel³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Fig. 1. Bone cells express Avprs. Immunofluorescence micrographs (A) and Western immunoblotting (B)show the expression of Avpr1α in osteoblasts and osteoclasts, and as a function of osteoblast (mineralization) and osteoclast (with Rankl) differentiation. The expression of Avp (ligand) and Avpr1α (receptor) in osteoblasts is regulated by 17β-estradiol, as determined by quantitative PCR (C) and Western immunoblotting (D). (Magnification: A, 63×.) Because Avp is a small peptide, its precursor neurophysin II is measured. Statistics: Student t test, P values shown compared with 0 h. Stimulation of Erk phosphorylation (p-Erk) as a function of total Erk (t-Erk) by Avp (10 −8 M) in osteoclast precursors (preosteoclasts), osteoclasts (OC), and osteoblasts establishes functionality of the Avpr1α in the presence or absence of the receptor inhibitor SR49059 (10 −8 M) (E). Western immunoblotting showing the expression of Avpr2 in preosteoclasts, OCs (F), and osteoblasts (G) isolated from Avpr1α −/− mice, as well as in MC3T3.E1 osteoblast precursors (G). Functionality of Avpr2 was confirmed by the demonstration that cells from Avpr1α −/− mice remained responsive to AVP in reducing the expression of osteoblast differentiation genes, namely Runx2, Osx, Bsp, Atf4, Opn, and Osteocalcin (quantitative PCR, P values shown) (H). Only relevant bands from Western blots are shown, with gaps introduced where empty lanes are excised to conserve space.

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Section: Kn-93 Reduces Ne-evoked Increases Of I Cal In Patients Withcontrasting

confidence: 54%

Arrhythmias, elicited by catecholamines and serotonin, vanish in human chronic atrial fibrillation

Christ

Rozmaritsa²,

Engel³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…Future studies are needed to assess how posttranslational modifications throughout the regulatory domain of CaMKII␦ synergize functionally to modulate Ca 2ϩ /CaM affinity. Inhibition of CaMKII␦ has been suggested as a potential therapeutic strategy for the prevention or amelioration of heart disease (35,36). Therefore, understanding the basic mechanisms that underlie CaMKII␦ activation and inhibition is critical for the development of future therapies.…”

Section: Discussionmentioning

confidence: 99%

S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ

Erickson

Nichols

Uchinoumi

et al. 2015

Journal of Biological Chemistry

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Background: CaMKII␦ and NO can modulate cardiac signaling/pathology. Results: NO treatment after calcium/calmodulin binding prolongs CaMKII␦ activation, whereas NO pretreatment inhibits CaMKII␦ activation, effects mediated by Cys-290 and Cys-273, respectively. Conclusion: S-nitrosylation has a dual role in modulating CaMKII␦ in the heart. Significance: Dual regulation by NO is a new pathway by which CaMKII can modulate cardiac function.

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“…Nox2 appears to be a promising target to tackle arrhythmia and calcium dysregulation related to enhanced angiotensin II signaling. 1,5,6 It seems clear that, in many settings, Nox4 mediates protective effects through specific redox signaling. Elucidation of the…”

Section: Article See P 643mentioning

confidence: 99%

Parsing the Role of NADPH Oxidase Enzymes and Reactive Oxygen Species in Heart Failure

Shah

2015

Circulation

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New Therapeutic Targets in Cardiology

Cited by 98 publications

References 127 publications

Arrhythmias, elicited by catecholamines and serotonin, vanish in human chronic atrial fibrillation

Arrhythmias, elicited by catecholamines and serotonin, vanish in human chronic atrial fibrillation

S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ

Parsing the Role of NADPH Oxidase Enzymes and Reactive Oxygen Species in Heart Failure

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