Xander H.T. Wehrens
Baylor College of Medicine
301 Papers
1.3K Citations
Xander H.T. Wehrens is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Ryanodine receptor 2 & Ryanodine receptor. The author has an hindex of 69, co-authored 252 publications. Previous affiliations of Xander H.T. Wehrens include Boston Children's Hospital & Cardiovascular Institute Hospital.
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Papers
Oxidized CaMKII and O-GlcNAcylation cause increased atrial fibrillation in diabetic mice by distinct mechanisms.
Olurotimi O. Mesubi,Adam G. Rokita,Neha Abrol,Yuejin Wu,Biyi Chen,Qinchuan Wang,Jonathan M. Granger,Anthony Tucker-Bartley,Elizabeth D. Luczak,Kevin R. Murphy,Priya Umapathi,Partha S. Banerjee,Tatiana Boronina,Robert N. Cole,Lars S. Maier,Xander H.T. Wehrens,Joel L. Pomerantz,Long-Sheng Song,Rexford S. Ahima,Gerald W. Hart,Natasha E. Zachara,Mark E. Anderson +21 more
TL;DR: It is shown that T1D and T2D significantly increased AF, and this increase required CaMKII and OGN, and it is suggested ROS primarily promotes AF by ox-CaMKII, while OGN promotesAF by a CaMK II-independent mechanism(s).
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Genetic inhibition of PKA phosphorylation of RyR2 prevents dystrophic cardiomyopathy
Satyam Sarma,Na Li,Ralph J. van Oort,Corey L. Reynolds,Darlene G. Skapura,Xander H.T. Wehrens +5 more
TL;DR: Inhibition of PKA phosphorylation of RyR2 reduced SR Ca2+ leak and attenuated cardiomyopathy in mdx mice, suggesting that enhanced PKAosphorylation at S2808 contributes to abnormal Ca 2+ homeostasis associated with dystrophic cardiopathy.
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Exercise restores dysregulated gene expression in a mouse model of arrhythmogenic cardiomyopathy
Sirisha Cheedipudi,Jinzhu Hu,Siyang Fan,Ping Yuan,Jennifer L. Karmouch,Grace Czernuszewicz,Matthew J. Robertson,Cristian Coarfa,Kui Hong,Yan Yao,Hanna Campbell,Xander H.T. Wehrens,Priyatansh Gurha,Ali J. Marian +13 more
TL;DR: Treadmill exercise restored transcript levels of the majority of dysregulated genes in cardiac myocytes, reduced myocardial apoptosis, and induced eccentric cardiac hypertrophy without affecting cardiac dysfunction in a mouse model of ACM, suggesting treadmill exercise might have partial salutary phenotypic effects in ACM.
Ranolazine prevents pressure overload-induced cardiac hypertrophy and heart failure by restoring aberrant Na+ and Ca2+ handling.
Jiali Nie,Quanlu Duan,Mengying He,Xianqing Li,Bei Wang,Chi Zhou,Lujin Wu,Zheng Wen,Chen Chen,Dao Wu Wang,Katherina M. Alsina,Xander H.T. Wehrens,Dao Wen Wang,Li Ni,Li Ni +14 more
TL;DR: The effects of ranolazine on pressure overload‐induced cardiac hypertrophy and heart failure in mice is investigated.
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Ryanodine receptor phosphorylation by oxidized CaMKII contributes to the cardiotoxic effects of cardiac glycosides
Hsiang-Ting Ho,Bin Liu,Jedidiah S. Snyder,Qing Lou,Elizabeth A. Brundage,Florencia Velez-Cortes,Honglan Wang,Mark T. Ziolo,Mark E. Anderson,Chandan K. Sen,Xander H.T. Wehrens,Vadim V. Fedorov,Brandon J. Biesiadecki,Thomas J. Hund,Sandor Gyorke +14 more
TL;DR: The results suggest that the arrhythmogenic adverse effects of CGs on Ca(2+) handling involve PI3K- and PKC-mediated stimulation of NOX2 and subsequent NoX2-dependent ROS release from the mitochondria; mitochondria-derived ROS then activate CaMKII with consequent phosphorylation of RyR2 at Ser 2814.
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