ArticleJournal of the American Heart Association2019
CTRP9 Ameliorates Atrial Inflammation, Fibrosis, and Vulnerability to Atrial Fibrillation in Post-Myocardial Infarction Rats.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 66 citations in OpenAlex.
- Association of plasma C1q/TNF-related protein 9 levels with disease severity and prognosis in patients with coronary atherosclerotic heart disease.Scientific reports · 2026Article
- Low-intensity pulsed ultrasound attenuates atrial remodelling and atrial fibrillation after myocardial infarction: an experimental pre-clinical study.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
- Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Review
- TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.Aging and disease · 2025Review
- Platelet-to-Lymphocyte Ratio as a Predictor of Atrial Fibrillation in STEMI Patients.Medical science monitor : international medical journal of experimental and clinical research · 2025Observational
- Interleukin-6: Molecular Mechanisms and Therapeutic Perspectives in Atrial Fibrillation.Current medical science · 2025Review
- Investigation of predictive parameters for recurrence in patients undergoing electrical cardioversion for atrial fibrillation.Journal of arrhythmia · 2025Article
- N-terminal domain of CTRP9 promotes cardiac fibroblast activation in myocardial infarction via Rap1/Mek/Erk pathway.Journal of translational medicine · 2025Article
- The gut microbial metabolite phenylacetylglutamine increases susceptibility to atrial fibrillation after myocardial infarction through ferroptosis and NLRP3 inflammasome.Apoptosis : an international journal on programmed cell death · 2025Article
- Advancing Atrial Fibrillation Research: The Role of Animal Models, Emerging Technologies and Translational Challenges.Biomedicines · 2025Review
- Construction and validation of a predictive model for new-onset atrial fibrillation in patients with acute myocardial infarction following emergency percutaneous coronary intervention based on novel inflammatory markers.Frontiers in cardiovascular medicine · 2025Article
- Predictive Potential of CRTP5 and SII for Coronary Artery Severity and Myocardial Fibrosis in Patients with NSTE-ACS: An Exploratory Biomarker Study.Journal of inflammation research · 2025Article
- The Potential Role of Cardiokines in Heart and Kidney Diseases.Current medicinal chemistry · 2025Review
- The SK4 channel allosteric blocker, BA6b9, reduces atrial fibrillation substrate in rats with reduced ejection fraction.PNAS nexus · 2024Article
- USP38 exacerbates atrial inflammation, fibrosis, and susceptibility to atrial fibrillation after myocardial infarction in mice.Molecular medicine (Cambridge, Mass.) · 2023Article
- Ubiquitin-specific protease 11-mediated CD36 deubiquitination acts on C1q/TNF-related protein 9 against atherosclerosis.ESC heart failure · 2023Article
- TRIM21 deficiency protects against atrial inflammation and remodeling post myocardial infarction by attenuating oxidative stress.Redox biology · 2023Article
- Candidate SNP Markers Significantly Altering the Affinity of TATA-Binding Protein for the Promoters of Human Hub Genes for Atherogenesis, Atherosclerosis and Atheroprotection.International journal of molecular sciences · 2023Article
- Complement 1q/Tumor Necrosis Factor-Related Proteins (CTRPs): Structure, Receptors and Signaling.Biomedicines · 2023Review
- Combining bioinformatics and machine learning to identify common mechanisms and biomarkers of chronic obstructive pulmonary disease and atrial fibrillation.Frontiers in cardiovascular medicine · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Inflammation and fibrosis play an important role in the pathogenesis of atrial fibrillation (AF) after myocardial infarction (MI). CTRP9 (C1q/tumor necrosis factor-related protein-9) as a secreted glycoprotein can reverse left ventricle remodeling post-MI, but its effects on MI-induced atrial inflammation, fibrosis, and associated AF are unknown. Methods and Results MI model rats received adenoviral supplementation of CTRP9 (Ad-CTRP9) by jugular-vein injection. Cardiac function, inflammatory, and fibrotic indexes and related signaling pathways, electrophysiological properties, and AF inducibility of atria in vivo and ex vivo were detected in 3 or 7 days after MI. shCTRP9 (short hairpin CTRP9) and shRNA were injected into rat and performed similar detection at day 5 or 10. Adverse atrial inflammation and fibrosis, cardiac dysfunction were induced in both MI and Ad-GFP (adenovirus-encoding green fluorescent protein)+MI rats. Systemic CTRP9 treatment improved cardiac dysfunction post-MI. CTRP9 markedly ameliorated macrophage infiltration and attenuated the inflammatory responses by downregulating interleukin-1β and interleukin-6, and upregulating interleukin-10, in 3 days post-MI; depressed left atrial fibrosis by decreasing the expressions of collagen types I and III, α-SMA, and transforming growth factor β1 in 7 days post-MI possibly through depressing the Toll-like receptor 4/nuclear factor-κB and Smad2/3 signaling pathways. Electrophysiologic recordings showed that increased AF inducibility and duration, and prolongation of interatrial conduction time induced by MI were attenuated by CTRP9; moreover, CTRP9 was negatively correlated with interleukin-1β and AF duration. Downregulation of CTRP9 aggravated atrial inflammation, fibrosis, susceptibility of AF and prolonged interatrial conduction time, without affecting cardiac function. Conclusions CTRP9 is effective at attenuating atrial inflammation and fibrosis, possibly via its inhibitory effects on the Toll-like receptor 4/nuclear factor-κB and Smad2/3 signaling pathways, and may be an original upstream therapy for AF in early phase of MI.
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