Disruption of Ca 2+ i Homeostasis and Connexin 43 Hemichannel Function in the Right Ventricle Precedes Overt Arrhythmogenic Cardiomyopathy in Plakophilin-2–Deficient Mice | Zendy

JoonChul Kim | Zendy; Marta Pérez-Hernández | Zendy; Francisco Alvarado | Zendy; Svetlana Maurya | Zendy; Jérôme Montnach | Zendy; Yandong Yin | Zendy; Mingliang Zhang | Zendy; Xianming Lin | Zendy; Carolina Vásquez | Zendy; Adriana Heguy | Zendy; FengXia Liang | Zendy; SunHee Woo | Zendy; Gregory E. Morley | Zendy; Eli Rothenberg | Zendy; Alicia Lundby | Zendy; Héctor H. Valdivia | Zendy; Marina Cerrone | Zendy; Mario Delmar | Zendy

Open Access

Disruption of Ca ²⁺ _i Homeostasis and Connexin 43 Hemichannel Function in the Right Ventricle Precedes Overt Arrhythmogenic Cardiomyopathy in Plakophilin-2–Deficient Mice

Author(s) -

JoonChul Kim,

Marta Pérez-Hernández,

Francisco Alvarado,

Svetlana Maurya,

Jérôme Montnach,

Yandong Yin,

Mingliang Zhang,

Xianming Lin,

Carolina Vásquez,

Adriana Heguy,

FengXia Liang,

SunHee Woo,

Gregory E. Morley,

Eli Rothenberg,

Alicia Lundby,

Héctor H. Valdivia,

Marina Cerrone,

Mario Delmar

Publication year - 2019

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.119.039710

Subject(s) - ventricle , myocyte , medicine , ryanodine receptor 2 , ryanodine receptor , connexin , cardiomyopathy , endoplasmic reticulum , endocrinology , gap junction , heart failure , cardiology , microbiology and biotechnology , calcium , biology , intracellular

Plakophilin-2 (PKP2) is classically defined as a desmosomal protein. Mutations in PKP2 associate with most cases of gene-positive arrhythmogenic right ventricular cardiomyopathy. A better understanding of PKP2 cardiac biology can help elucidate the mechanisms underlying arrhythmic and cardiomyopathic events consequent to PKP2 deficiency. Here, we sought to capture early molecular/cellular events that can act as nascent arrhythmic/cardiomyopathic substrates.

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