ArticlePloS one2011
Lack of chemokine signaling through CXCR5 causes increased mortality, ventricular dilatation and deranged matrix during cardiac pressure overload.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Proteomics for heart failure risk stratification: a systematic review.BMC medicine · 2024Pooled it
- The Role of Chemokines and Small Leucine-Rich Proteoglycans in Cardiac Remodeling in Immunosuppressant-Treated Male Rats.International journal of molecular sciences · 2025Article
- Homeostatic Role of Decorin in Right Ventricular Pressure Overload and Pulmonary Hypertension Induced Remodeling.JACC. Basic to translational science · 2025Article
- IL-17 is associated with disease severity and targetable inflammatory processes in heart failure.ESC heart failure · 2024Article
- Cardiac Molecular Analysis Reveals Aging-Associated Metabolic Alterations Promoting Glycosaminoglycans Accumulation via Hexosamine Biosynthetic Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cardiac Molecular Analysis Reveals Aging-Associated Metabolic Alterations Promoting Glycosaminoglycans Accumulation Via Hexosamine Biosynthetic Pathway.bioRxiv : the preprint server for biology · 2023Article
- Identification of diagnostic immune-related gene biomarkers for predicting heart failure after acute myocardial infarction.Open medicine (Warsaw, Poland) · 2023Article
- The role of fibromodulin in inflammatory responses and diseases associated with inflammation.Frontiers in immunology · 2023Review
- Asporin, an extracellular matrix protein, is a beneficial regulator of cardiac remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Left ventricular assist device bioinformatics identify possible hubgenes and regulatory networks involved in the myocardium of patients with left ventricular assist device.Frontiers in cardiovascular medicine · 2022Article
- Predicting the Key Genes Involved in Aortic Valve Calcification Through Integrated Bioinformatics Analysis.Frontiers in genetics · 2021Article
- RNA-seq data from C-X-C chemokine receptor type 5 (CXCR5) gene knockout aged mice with retinal degeneration phenotype.Data in brief · 2020Article
- Moderate Loss of the Extracellular Matrix Proteoglycan Lumican Attenuates Cardiac Fibrosis in Mice Subjected to Pressure Overload.Cardiology · 2020Article
- Autoimmune-Mediated Retinopathy in CXCR5-Deficient Mice as the Result of Age-Related Macular Degeneration Associated Proteins Accumulation.Frontiers in immunology · 2019Article
- CXCL13 polymorphism is associated with essential hypertension in Tatars from Russia.Molecular biology reports · 2018Article
- Article
- The Human Blood-Nerve Barrier Transcriptome.Scientific reports · 2017Article
- Chemokines and Heart Disease: A Network Connecting Cardiovascular Biology to Immune and Autonomic Nervous Systems.Mediators of inflammation · 2016Review
- Lumican deficiency results in cardiomyocyte hypertrophy with altered collagen assembly.Journal of molecular and cellular cardiology · 2015Article
- Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleInflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. Based on their role in inflammation and matrix remodeling in other tissues, we hypothesized that CXCL13 and CXCR5 could be involved in cardiac remodeling during HF.
objectiveWe sought to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF. METHODS AND
resultsMice harboring a systemic knockout of the CXCR5 (CXCR5(-/-)) displayed increased mortality during a follow-up of 80 days after aortic banding (AB). Following three weeks of AB, CXCR5(-/-) developed significant left ventricular (LV) dilatation compared to wild type (WT) mice. Microarray analysis revealed altered expression of several small leucine-rich proteoglycans (SLRPs) that bind to collagen and modulate fibril assembly. Protein levels of fibromodulin, decorin and lumican (all SLRPs) were significantly reduced in AB CXCR5(-/-) compared to AB WT mice. Electron microscopy revealed loosely packed extracellular matrix with individual collagen fibers and small networks of proteoglycans in AB CXCR5(-/-) mice. Addition of CXCL13 to cultured cardiac fibroblasts enhanced the expression of SLRPs. In patients with HF, we observed increased myocardial levels of CXCR5 and SLRPs, which was reversed following LV assist device treatment.
conclusionsLack of CXCR5 leads to LV dilatation and increased mortality during pressure overload, possibly via lack of an increase in SLRPs. This study demonstrates a critical role of the chemokine CXCL13 and CXCR5 in survival and maintaining of cardiac structure upon pressure overload, by regulating proteoglycans essential for correct collagen assembly.
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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.