ArticleAmerican journal of physiology. Heart and circulatory physiology2016
LRRC10 is required to maintain cardiac function in response to pressure overload.
Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Rac1 palmitoylation is required for cardiac stress adaptation and regulation of protein kinase A signaling.JCI insight · 2025Article
- Cardiomyocyte Janus kinase 1 (JAK1) signaling is required for cardiac homeostasis and cytokine-dependent activation of STAT3.Journal of molecular and cellular cardiology · 2025Article
- Rab3gap1 palmitoylation cycling modulates cardiomyocyte exocytosis and atrial natriuretic peptide release.Biophysical journal · 2025Article
- Probing the CabioRxiv : the preprint server for biology · 2025Article
- The mechanism of CaThe Journal of biological chemistry · 2025Article
- Cardiac L-type calcium channel regulation by Leucine-Rich Repeat-Containing Protein 10.Channels (Austin, Tex.) · 2024Review
- A genetically encoded actuator boosts L-type calcium channel function in diverse physiological settings.Science advances · 2024Article
- Disruption of the nuclear localization signal in RBM20 is causative in dilated cardiomyopathy.JCI insight · 2023Article
- zDHHC9 Regulates Cardiomyocyte Rab3a Activity and Atrial Natriuretic Peptide Secretion Through Palmitoylation of Rab3gap1.JACC. Basic to translational science · 2023Article
- RBM20 phosphorylation and its role in nucleocytoplasmic transport and cardiac pathogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- EGR1 Is Implicated in Right Ventricular Cardiac Remodeling Associated with Pulmonary Hypertension.Biology · 2022Article
- RBM20Journal of molecular and cellular cardiology · 2022Article
- Multi-omics assessment of dilated cardiomyopathy using non-negative matrix factorization.PloS one · 2022Article
- Genetic Loss ofCirculation. Arrhythmia and electrophysiology · 2020Article
- Disruption of valosin-containing protein activity causes cardiomyopathy and reveals pleiotropic functions in cardiac homeostasis.The Journal of biological chemistry · 2019Article
- A 6-Gene Risk Signature Predicts Survival of Glioblastoma Multiforme.BioMed research international · 2019Article
- Defective Flux of Thrombospondin-4 through the Secretory Pathway Impairs Cardiomyocyte Membrane Stability and Causes Cardiomyopathy.Molecular and cellular biology · 2018Article
- Pediatric Dilated Cardiomyopathy-AssociatedJournal of the American Heart Association · 2018Article
- LRRC10 (Leucine-Rich Repeat Containing Protein 10) and REEP5 (Receptor Accessory Protein 5) as Novel Regulators of Cardiac Excitation-Contraction Coupling Structure and Function.Journal of the American Heart Association · 2018Article
- Genome-Wide Temporal Profiling of Transcriptome and Open Chromatin of Early Cardiomyocyte Differentiation Derived From hiPSCs and hESCs.Circulation research · 2017Article
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Abstract
We previously reported that the cardiomyocyte-specific leucine-rich repeat containing protein (LRRC)10 has critical functions in the mammalian heart. In the present study, we tested the role of LRRC10 in the response of the heart to biomechanical stress by performing transverse aortic constriction on Lrrc10-null (Lrrc10(-/-)) mice. Mild pressure overload induced severe cardiac dysfunction and ventricular dilation in Lrrc10(-/-) mice compared with control mice. In addition to dilation and cardiomyopathy, Lrrc10(-/-) mice showed a pronounced increase in heart weight with pressure overload stimulation and a more dramatic loss of cardiac ventricular performance, collectively suggesting that the absence of LRRC10 renders the heart more disease prone with greater hypertrophy and structural remodeling, although rates of cardiac fibrosis and myocyte dropout were not different from control mice. Lrrc10(-/-) cardiomyocytes also exhibited reduced contractility in response to β-adrenergic stimulation, consistent with loss of cardiac ventricular performance after pressure overload. We have previously shown that LRRC10 interacts with actin in the heart. Here, we show that His(150) of LRRC10 was required for an interaction with actin, and this interaction was reduced after pressure overload, suggesting an integral role for LRRC10 in the response of the heart to mechanical stress. Importantly, these experiments demonstrated that LRRC10 is required to maintain cardiac performance in response to pressure overload and suggest that dysregulated expression or mutation of LRRC10 may greatly sensitize human patients to more severe cardiac disease in conditions such as chronic hypertension or aortic stenosis.
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