ArticleThe Journal of clinical investigation2023
Pressure overload induces ISG15 to facilitate adverse ventricular remodeling and promote heart failure.
Article in The Journal of clinical investigation, 2023. 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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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
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- Consensus statement on mass spectrometry-based proteomic analysis of cardiac tissue.Nature cardiovascular research · 2026Article
- METTL14-dependent mbioRxiv : the preprint server for biology · 2026Article
- Stimulator of Interferon Genes Is a Fine-Tuner, but Not a Prime Mover, of Kidney Inflammation.The American journal of pathology · 2026Article
- When ISG15 is involved in inflammation.Frontiers in immunology · 2026Review
- Targeting the ISG15+STAT1+ monocyte-driven inflammatory storm with Fedratinib in traumatic lung injury via the JAK2/STAT3/PIM1 axis.Frontiers in immunology · 2026Article
- Biphasic actions of the adenosine A2a receptor antagonist istradefylline in mice with obstructive uropathy.Scientific reports · 2025Article
- Involvement of TGF-β, mTOR, and inflammatory mediators in aging alterations during myxomatous mitral valve disease in a canine model.GeroScience · 2025Review
- Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 2025Review
- Deciphering the transcriptomic landscape of systemic lupus erythematosus-associated pulmonary arterial hypertension.Respiratory research · 2025Article
- Roles of Autophagy, Mitophagy, and Mitochondria in Left Ventricular Remodeling after Myocardial Infarction.Reviews in cardiovascular medicine · 2025Review
- ISGylation: is our genome yearning for such a modification?Acta biochimica et biophysica Sinica · 2025Review
- Single-cell transcriptomics unravels the early immune landscape of renal allograft rejection and nominates Ccl3-Ccr5 as a therapeutic target.Frontiers in immunology · 2025Article
- Heart Failure Is Closely Associated With the Expression Characteristics of Type I Interferon-Related Genes.Clinical cardiology · 2025Article
- Macrophages suppress cardiac reprogramming of fibroblasts in vivo via IFN-mediated intercellular self-stimulating circuit.Protein & cell · 2024Article
- Left atrial single-cell transcriptomics reveals amphiregulin as a surrogate marker for atrial fibrillation.Communications biology · 2024Article
- Interferons and interferon-related pathways in heart disease.Frontiers in cardiovascular medicine · 2024Review
- Cardiometabolic Modulation by Semaglutide Contributes to Cardioprotection in Rats with Myocardial Infarction.Drug design, development and therapy · 2024Article
- SARS-CoV-2 spike receptor-binding domain is internalized and promotes protein ISGylation in human induced pluripotent stem cell-derived cardiomyocytes.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
Inflammation promotes adverse ventricular remodeling, a common antecedent of heart failure. Here, we set out to determine how inflammatory cells affect cardiomyocytes in the remodeling heart. Pathogenic cardiac macrophages induced an IFN response in cardiomyocytes, characterized by upregulation of the ubiquitin-like protein IFN-stimulated gene 15 (ISG15), which posttranslationally modifies its targets through a process termed ISGylation. Cardiac ISG15 is controlled by type I IFN signaling, and ISG15 or ISGylation is upregulated in mice with transverse aortic constriction or infused with angiotensin II; rats with uninephrectomy and DOCA-salt, or pulmonary artery banding; cardiomyocytes exposed to IFNs or CD4+ T cell-conditioned medium; and ventricular tissue of humans with nonischemic cardiomyopathy. By nanoscale liquid chromatography-tandem mass spectrometry, we identified the myofibrillar protein filamin-C as an ISGylation target. ISG15 deficiency preserved cardiac function in mice with transverse aortic constriction and led to improved recovery of mouse hearts ex vivo. Metabolomics revealed that ISG15 regulates cardiac amino acid metabolism, whereas ISG15 deficiency prevented misfolded filamin-C accumulation and induced cardiomyocyte autophagy. In sum, ISG15 upregulation is a feature of pathological ventricular remodeling, and protein ISGylation is an inflammation-induced posttranslational modification that may contribute to heart failure development by altering cardiomyocyte protein turnover.
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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 Socratic graph.