ArticlePloS one2021
CX3CR1 is a prerequisite for the development of cardiac hypertrophy and left ventricular dysfunction in mice upon transverse aortic constriction.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Experimental study on the role and biomarker potential of CX3CR1 in osteoarthritis.Annals of medicine · 2025Article
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- Hypertrophic heart failure promotes gut dysbiosis and gut leakage in interleukin 10-deficient mice.American journal of physiology. Heart and circulatory physiology · 2025Article
- Article
- Identification of key genes for heart failure in dilated cardiomyopathy in different populations.Frontiers in genetics · 2025Article
- Cardiac radiation improves ventricular function in mice and humans with cardiomyopathy.Med (New York, N.Y.) · 2023Article
- Fractalkine Signalling (CXJournal of clinical medicine · 2023Review
- Review
- Eosinophils protect pressure overload- and β-adrenoreceptor agonist-induced cardiac hypertrophy.Cardiovascular research · 2023Article
- Article
- Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling.Frontiers in cell and developmental biology · 2021Review
- CX3CR1 Acts as a Protective Biomarker in the Tumor Microenvironment of Colorectal Cancer.Frontiers in immunology · 2021Article
- Characterization of Transverse Aortic Constriction in Mice Based on the Specific Recruitment of Leukocytes to the Hypertrophic Myocardium and the Aorta Ascendens.Mediators of inflammation · 2021Article
- Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CX3CL1/CX3CR1 axis mediates recruitment and extravasation of CX3CR1-expressing subsets of leukocytes and plays a pivotal role in the inflammation-driven pathology of cardiovascular disease. The cardiac immune response differs depending on the underlying causes. This suggests that for the development of successful immunomodulatory therapy in heart failure due to chronic pressure overload induced left ventricular (LV) hypertrophy, the underlying immune patterns must be examined. Here, the authors demonstrate that Fraktalkine-receptor CX3CR1 is a prerequisite for the development of cardiac hypertrophy and left ventricular dysfunction in a mouse model of transverse aortic constriction (TAC). The comparison of C57BL/6 mice with CX3CR1 deficient mice displayed reduced LV hypertrophy and preserved cardiac function in response to pressure overload in mice lacking CX3CR1. Moreover, the normal immune response following TAC induced pressure overload which is dominated by Ly6Clow macrophages changed to an early pro-inflammatory immune response driven by neutrophils, Ly6Chigh macrophages and altered cytokine expression pattern in CX3CR1 deficient mice. In this early inflammatory phase of LV hypertrophy Ly6Chigh monocytes infiltrated the heart in response to a C-C chemokine ligand 2 burst. CX3CR1 expression impacts the immune response in the development of LV hypertrophy and its absence has clear cardioprotective effects. Hence, suppression of CX3CR1 may be an important immunomodulatory therapeutic target to ameliorate pressure-overload induced heart failure.
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