ArticleEBioMedicine2020
Elevated myocardial SORBS2 and the underlying implications in left ventricular noncompaction cardiomyopathy.
Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- SORBS2: A Molecular Nexus in Multisystem Diseases Through Scaffold-Mediated Regulation.Journal of cellular and molecular medicine · 2026Review
- Long noncoding RNA SRRM2-AS1 mediates coronary artery damage in Kawasaki disease by promoting endothelial-to-mesenchymal transition.Clinical and experimental medicine · 2026Article
- Roles of autophagy in sepsis-induced myocardial dysfunction: a comprehensive review.American journal of translational research · 2026Review
- Multi-omics study of molecular and genetic bases of orthostatic hypotension.Clinical epigenetics · 2025Article
- Impact of Sorbs2 dysfunction on cardiovascular diseases.Biochimica et biophysica acta. Molecular basis of disease · 2025Review
- Cardiomyocyte SORBS2 expression increases in heart failure and regulates integrin interactions and extracellular matrix composition.Cardiovascular research · 2025Article
- Left atrial single-cell transcriptomics reveals amphiregulin as a surrogate marker for atrial fibrillation.Communications biology · 2024Article
- Deciphering mechanisms of cardiomyocytes and non-cardiomyocyte transformation in myocardial remodeling of permanent atrial fibrillation.Journal of advanced research · 2024Article
- Cellular-level analyses ofBiochemistry and biophysics reports · 2024Article
- Article
- SORBS2 upregulation may contribute to dysfunction in LVNC via the Notch pathway.Acta biochimica et biophysica Sinica · 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
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- SORBS2 as a molecular target for atherosclerosis in patients with familial hypercholesterolemia.Journal of translational medicine · 2022Article
- The interaction protein of SORBS2 in myocardial tissue to find out the pathogenic mechanism of LVNC disease.Aging · 2022Article
- Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice.Oxidative medicine and cellular longevity · 2022Article
- Changes in ion channel expression and function associated with cardiac arrhythmogenic remodeling by Sorbs2.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
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- Article
- Effects of CMYA1 overexpression on cardiac structure and function in mice.Acta biochimica et biophysica Sinica · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLeft ventricular noncompaction cardiomyopathy (LVNC) is a hereditary heart disease characterized by an excessive trabecular meshwork of deep intertrabecular recesses within the ventricular myocardium. The guidelines for management of LVNC patients aim to improve quality of life by preventing cardiac heart failure. However, the mechanism underlying LVNC-associated heart failure remains poorly understood.
methodsUsing protein mass spectrometry analysis, we established that Sorbin And SH3 Domain Containing 2 (SORBS2) is up-regulated in LVNC hearts without changes to structure proteins. We conducted in vivo experiments wherein the heart tissues of wild-type mice were injected with an AAV9 vector to overexpress SORBS2, followed by analysis using echocardiography, T-tubule analysis and Ca
findingsLVNC myocardial tissues feature strongly elevated expression of SORBS2, microtubule densification and redistribution of Junctophilin 2 (JP2). SORBS2 interacts with β-tubulin, promoting its polymerization in 293T cells and hESC-derived CMs. In vivo, cardiac dysfunction, β-tubulin densification, JP2 translocation, T-tubule disorganization and Ca
interpretationWe identified a novel mechanism through which SORBS2 interacts with β-tubulin and promotes microtubule densification, eventually effecting JP2 distribution and T-tubule, potentially contributing to heart failure in LVNC disease. FUND: This work was supported by a CAMS Initiative for Innovative Medicine grant (CAMS-I2M, 2016-I2M-1-015 to Y.J.Wei).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.