ArticleCirculation2011
Absence of SOCS3 in the cardiomyocyte increases mortality in a gp130-dependent manner accompanied by contractile dysfunction and ventricular arrhythmias.
Article in Circulation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- The multifaceted role of SOCS3 in colorectal cancer: molecular mechanisms and clinical implications.Molecular biology reports · 2026Review
- Role of CR6-Interacting Factor 1 (Crif1) in Cardiac Mitochondrial Structure and Stress-Induced Functional Decline.Korean circulation journal · 2026Article
- GP130 Antagonism Enhances Porcine RV Function.Circulation research · 2025Article
- Identification of a key smooth muscle cell subset driving ischemic cardiomyopathy progression through single-cell RNA sequencing.Scientific reports · 2025Article
- Glycoprotein 130 Antagonism Counteracts Metabolic and Inflammatory Alterations to Enhance Right Ventricle Function in Pulmonary Artery Banded Pigs.bioRxiv : the preprint server for biology · 2025Article
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- Article
- Response by Prisco and Prins to Letter Regarding Article, "Inflammatory Glycoprotein 130 Signaling Links Changes in Microtubules and Junctophilin-2 to Altered Mitochondrial Metabolism and Right Ventricular Contractility".Circulation. Heart failure · 2022Article
- Compound heterozygous mutation of the ASXL3 gene causes autosomal recessive congenital heart disease.Human genetics · 2021Article
- Phosphoproteomic Analysis Reveals Downstream PKA Effectors of AKAP Cypher/ZASP in the Pathogenesis of Dilated Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Article
- SOCS3 Negatively Regulates Cardiac Hypertrophy via Targeting GRP78-Mediated ER Stress During Pressure Overload.Frontiers in cell and developmental biology · 2021Article
- Emerging therapeutic targets for cardiac arrhythmias: role of STAT3 in regulating cardiac fibroblast function.Expert opinion on therapeutic targets · 2021Review
- Pathogenesis of SARS-CoV-2 induced cardiac injury from the perspective of the virus.Journal of molecular and cellular cardiology · 2020Article
- The role of interleukin-6 in intracellular signal transduction after chronic β-adrenergic stimulation in mouse myocardium.Archives of medical science : AMS · 2019Article
- Therapeutic Delivery of miR-148a Suppresses Ventricular Dilation in Heart Failure.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- βIV-Spectrin regulates STAT3 targeting to tune cardiac response to pressure overload.The Journal of clinical investigation · 2018Article
- Interaction of suppressor of cytokine signalling 3 with cavin-1 links SOCS3 function and cavin-1 stability.Nature communications · 2018Article
- Epigenome-wide association analysis revealed that SOCS3 methylation influences the effect of cumulative stress on obesity.Biological psychology · 2018Article
- Recent advances of adapter proteins in the regulation of heart diseases.Heart failure reviews · 2017Review
- Methylation and microRNA-mediated epigenetic regulation of SOCS3.Molecular biology reports · 2015Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSuppressor of cytokine signaling-3 (SOCS3) is a key negative-feedback regulator of the gp130 receptor that provides crucial signaling for cardiac hypertrophy and survival; however, an in vivo role of SOCS3 regulation on cardiac gp130 signaling remains obscure. METHODS AND
resultsWe generated cardiac-specific SOCS3 knockout (SOCS3 cKO) mice. These mice showed increased activation of gp130 downstream signaling targets (STAT3, ERK1/2, AKT, and p38) from 15 weeks of age and developed cardiac dysfunction from approximately 25 weeks of age with signs of heart failure. Surprisingly, SOCS3 cKO failing hearts had minimal histological abnormalities with intact myofibril ultrastructure. In addition, Ca(2+) transients were significantly increased in SOCS3 cKO failing hearts compared with wild-type hearts. We also found that Ser23/24 residues of troponin I were hypophosphorylated in SOCS3 cKO hearts before the manifestation of cardiac dysfunction. These data suggested the presence of abnormalities in myofilament Ca(2+) sensitivity in SOCS3 cKO mice. In addition to the contractile dysfunction, we found various ventricular arrhythmias in SOCS3 cKO nonfailing hearts accompanied by a sarcoplasmic reticulum Ca(2+) overload. To determine the contribution of gp130 signaling to the cardiac phenotype that occurs with SOCS3 deficiency, we generated cardiac-specific gp130 and SOCS3 double KO mice. Double KO mice lived significantly longer and had different histological abnormalities when compared with SOCS3 cKO mice, thus demonstrating the importance of gp130 signaling in the SOCS3 cKO cardiac phenotype.
conclusionsOur results demonstrate an important role of SOCS3 regulation on cardiac gp130 signaling in the pathogenesis of contractile dysfunction and ventricular arrhythmias.
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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.