ArticlePloS one2017
Mononuclear Phagocytes Are Dispensable for Cardiac Remodeling in Established Pressure-Overload Heart Failure.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 63 citations in OpenAlex.
- Immune cell signature in non-ischemic heart failure indicates chronic systemic immune activation with features of immunosenescence.Immunity & ageing : I & A · 2026Article
- Article
- Splenic CD23+ B Cells: Preventing Adverse Remodeling by Limiting IgE Production.Circulation research · 2025Article
- Experimental pressure overload induces a cardiac neoantigen specific humoral immune response.Journal of molecular and cellular cardiology · 2025Article
- Myocardial Inflammation in Heart Failure With Reduced and Preserved Ejection Fraction.Circulation research · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Neutrophils are indispensable for adverse cardiac remodeling in heart failure.Journal of molecular and cellular cardiology · 2024Article
- Mitochondrial Impairment: A Link for Inflammatory Responses Activation in the Cardiorenal Syndrome Type 4.International journal of molecular sciences · 2023Review
- Blood Immune Cell Alterations in Patients with Hypertensive Left Ventricular Hypertrophy and Heart Failure with Preserved Ejection Fraction.Journal of cardiovascular development and disease · 2023Article
- Immune Cells in Cardiac Injury Repair and Remodeling.Current cardiology reports · 2023Review
- OSMR deficiency aggravates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling.Journal of translational medicine · 2023Article
- Eosinophils protect pressure overload- and β-adrenoreceptor agonist-induced cardiac hypertrophy.Cardiovascular research · 2023Article
- Article
- Cardiorenal syndrome: long road between kidney and heart.Heart failure reviews · 2022Review
- Myocardial injury, troponin release, and cardiomyocyte death in brief ischemia, failure, and ventricular remodeling.American journal of physiology. Heart and circulatory physiology · 2022Review
- Role of CCR2-Positive Macrophages in Pathological Ventricular Remodelling.Biomedicines · 2022Review
- The heart under pressure: immune cells in fibrotic remodeling.Current opinion in physiology · 2022Article
- Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Resident Macrophages in the Heart: Cardioprotective Under Pressure.Circulation research · 2021Article
- The Macrophage Iron Signature in Health and Disease.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlthough cardiac and splenic mononuclear phagocytes (MPs), i.e., monocytes, macrophages and dendritic cells (DCs), are key contributors to cardiac remodeling after myocardial infarction, their role in pressure-overload remodeling is unclear. We tested the hypothesis that these immune cells are required for the progression of remodeling in pressure-overload heart failure (HF), and that MP depletion would ameliorate remodeling. METHODS AND
resultsC57BL/6 mice were subjected to transverse aortic constriction (TAC) or sham operation, and assessed for alterations in MPs. As compared with sham, TAC mice exhibited expansion of circulating LyC6hi monocytes and pro-inflammatory CD206- cardiac macrophages early (1 w) after pressure-overload, prior to significant hypertrophy and systolic dysfunction, with subsequent resolution during chronic HF. In contrast, classical DCs were expanded in the heart in a biphasic manner, with peaks both early, analogous to macrophages, and late (8 w), during established HF. There was no significant expansion of circulating DCs, or Ly6C+ monocytes and DCs in the spleen. Periodic systemic MP depletion from 2 to 16 w after TAC in macrophage Fas-induced apoptosis (MaFIA) transgenic mice did not alter cardiac remodeling progression, nor did splenectomy in mice with established HF after TAC. Lastly, adoptive transfer of splenocytes from TAC HF mice into naïve recipients did not induce immediate or long-term cardiac dysfunction in recipient mice.
conclusionsMononuclear phagocytes populations expand in a phasic manner in the heart during pressure-overload. However, they are dispensable for the progression of remodeling and failure once significant hypertrophy is evident and blood monocytosis has normalized.
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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.