ArticleBiochimica et biophysica acta. Molecular basis of disease2021
Changes in ion channel expression and function associated with cardiac arrhythmogenic remodeling by Sorbs2.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 13 citations in OpenAlex.
- Propafenone-mediated gap junctional uncoupling results from aberrant connexin-43 trafficking.Pharmacological reports : PR · 2026Article
- Intracellular Ionic Remodeling During Fetal Development of Hereditary Cardiomyopathy of the Hamster.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- SORBS2: A Molecular Nexus in Multisystem Diseases Through Scaffold-Mediated Regulation.Journal of cellular and molecular medicine · 2026Review
- Impact of Sorbs2 dysfunction on cardiovascular diseases.Biochimica et biophysica acta. Molecular basis of disease · 2025Review
- Comparative RNA-Seq analysis of differentially expressed genes in the sertoli cells of yak and cattle-yak.BMC veterinary research · 2025Article
- Roles of TRPM channels in glioma.Cancer biology & therapy · 2024Review
- The network of cardiac KNaunyn-Schmiedeberg's archives of pharmacology · 2024Review
- In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models.Cells · 2024Review
- Sorbs2 Deficiency and Vascular BK Channelopathy in Diabetes.Circulation research · 2024Article
- Inhibition of the voltage-gated potassium channel Kv1.5 by hydrogen sulfide attenuates remodeling through S-nitrosylation-mediated signaling.Communications biology · 2023Article
- Effects of Electrical Remodeling on Atrial Fibrillation in Diabetes Mellitus.Reviews in cardiovascular medicine · 2023Review
- TRPC6 N338S is a gain-of-function mutant identified in patient with doxorubicin-induced cardiotoxicity.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Knockout of Sorbin And SH3 Domain Containing 2 (Sorbs2) in Cardiomyocytes Leads to Dilated Cardiomyopathy in Mice.Journal of the American Heart Association · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The Sorbin and SH3 domain-containing protein 2 (Sorbs2) is an important component of cardiomyocyte sarcomere. It has been recently reported that loss of Sorbs2 is causally associated with arrhythmogenic cardiomyopathy in human. However, the ionic mechanisms leading to cardiac arrhythmogenesis by Sorbs2 deficiency are unknown. In this study, we hypothesized that Sorbs2 plays an important role in regulating cardiac ion channel expression and function. Using electrophysiological and molecular biological approaches, we found that the Sorbs2 knockout (KO) mice progressively developed cardiac structural and electrical remodeling as early as 1 to 2 months of age and died prematurely at 5 to 7 months of age. Electrocardiographic recordings showed that Sorbs2 KO mice had conduction delays, spontaneous ventricular extrasystoles and polymorphic ventricular tachyarrhythmia. Intracellular recordings revealed abnormal action potentials with depolarized resting potential, reduced upstroke velocity, prolonged repolarization, and effective refractory period in the ventricular preparations of Sorbs2 KO mice. Patch clamp experiments demonstrated that Sorbs2 KO mice displayed distinct abnormalities in the expression and function of cardiac ion channels, including those of the voltage-gated Na
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