ArticleBasic research in cardiology2020
Deletion of obscurin immunoglobulin domains Ig58/59 leads to age-dependent cardiac remodeling and arrhythmia.
Article in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- A Decrease in the Content of Giant Obscurin Isoform during the Development of Isoprenaline-Induced Myocardial Injury in Rats.Bulletin of experimental biology and medicine · 2025Article
- Novel compound heterozygous OBSCN variants in Chinese children with congenital pulmonary airway malformation.Italian journal of pediatrics · 2025Article
- Loss of OBSCN expression promotes bladder cancer progression but enhances the efficacy of PD-L1 inhibitors.Cell & bioscience · 2025Article
- Sex Chromosomes and Sex Hormones: Dissecting the Forces That Differentiate Female and Male Hearts.Circulation · 2025Review
- Constitutive deletion of the obscurin-Ig58/59 domains induces atrial remodeling and Ca2+-based arrhythmogenesis.JCI insight · 2025Article
- LncRNA CCRR maintains CaScience China. Life sciences · 2024Article
- Essential role of obscurin kinase-1 in cardiomyocyte coupling via N-cadherin phosphorylation.JCI insight · 2024Article
- Structural and signaling proteins in the Z-disk and their role in cardiomyopathies.Frontiers in physiology · 2023Review
- Alterations in cytoskeletal and CaFrontiers in cardiovascular medicine · 2023Article
- Editorial: Molecular and cellular mechanisms of heart failure: pathophysiology, pathogenesis and therapeutics.Frontiers in cardiovascular medicine · 2023Article
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Mitophagy alleviates ischemia/reperfusion-induced microvascular damage through improving mitochondrial quality control.Bioengineered · 2022Article
- Melatonin Attenuates Ischemia/Reperfusion-Induced Oxidative Stress by Activating Mitochondrial Fusion in Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Article
- Titin M-line insertion sequence 7 is required for proper cardiac function in mice.Journal of cell science · 2021Article
- Obscurin: A multitasking giant in the fight against cancer.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- Exploring Obscurin and SPEG Kinase Biology.Journal of clinical medicine · 2021Article
- Irisin Attenuates Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in the H9C2 Cellular Model of Septic Cardiomyopathy through Augmenting Fundc1-Dependent Mitophagy.Oxidative medicine and cellular longevity · 2021Article
- LATS2 Deletion Attenuates Myocardial Ischemia-Reperfusion Injury by Promoting Mitochondrial Biogenesis.Oxidative medicine and cellular longevity · 2021Article
- Mst2 Overexpression Inhibits Thyroid Carcinoma Growth and Metastasis by Disrupting Mitochondrial Fitness and Endoplasmic Reticulum Homeostasis.Journal of oncology · 2021Article
- Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress.Journal of oncology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Obscurin comprises a family of giant modular proteins that play key structural and regulatory roles in striated muscles. Immunoglobulin domains 58/59 (Ig58/59) of obscurin mediate binding to essential modulators of muscle structure and function, including canonical titin, a smaller splice variant of titin, termed novex-3, and phospholamban (PLN). Importantly, missense mutations localized within the obscurin-Ig58/59 region that affect binding to titins and/or PLN have been linked to the development of myopathy in humans. To elucidate the pathophysiological role of this region, we generated a constitutive deletion mouse model, Obscn-ΔIg58/59, that expresses obscurin lacking Ig58/59, and determined the consequences of this manipulation on cardiac morphology and function under conditions of acute stress and through the physiological process of aging. Our studies show that young Obscn-ΔIg58/59 mice are susceptible to acute β-adrenergic stress. Moreover, sedentary Obscn-ΔIg58/59 mice develop left ventricular hypertrophy that progresses to dilation, contractile impairment, atrial enlargement, and arrhythmia as a function of aging with males being more affected than females. Experiments in ventricular cardiomyocytes revealed altered Ca
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Registered trials
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.