ArticleCirculation research2016
Proliferation and Recruitment Contribute to Myocardial Macrophage Expansion in Chronic Heart Failure.
Open access · bronzeAbstract read
In one paragraph
Article in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 papers, 2 of them syntheses that pooled it.
0numbers the graph read from it
0cells of the map it votes in
283citing papers in PubMed, 2 pooled it
28.3field-weighted citation impact, top 1% of its field
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
283 citing papers in PubMed, 2 syntheses or guidelines pooled it, 413 citations in OpenAlex.
- Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023Pooled it
- Association of immune cell subsets with incident heart failure in two population-based cohorts.ESC heart failure · 2022Pooled it
- Optimized cardiac leukocyte isolation for flow cytometry enumeration and sorting.American journal of physiology. Heart and circulatory physiology · 2026Article
- Lactylation at the metabolic-epigenetic interface in cardiovascular diseases: context-dependent mechanisms and translational roadmap.Journal of advanced research · 2026Review
- MiR-378a-3p Promotes Macrophage Polarization from M1 to M2 for Cardiac Repair after Infarction Via Trem1.Journal of cardiovascular translational research · 2026Article
- Disruption of the brain-spleen axis impairs monocyte-microglia communication and accelerates disease progression in a mouse model of amyloidosis.Nature communications · 2026Article
- Bioinformatics Identification and Molecular Docking Validation of Post-Translational Modification-Related Hub Genes as Diagnostic Biomarkers and Therapeutic Targets in Myocardial Fibrosis.International journal of molecular sciences · 2026Article
- Association between the systemic inflammatory response index and 1-year all-cause mortality in intensive care unit patients with heart failure: a retrospective cohort study.Journal of thoracic disease · 2026Article
- Renal denervation attenuates cardiac fibrosis and improves left ventricular function in rats with myocardial infarction.Scientific reports · 2026Article
- E3 ubiquitin ligase TRIM21-mediated K48-linked ubiquitination of ALDH2 rs671 mutant promotes adverse cardiac remodeling.JCI insight · 2026Article
- Activation of α7nAChR prevents maladaptive right ventricular remodeling via inhibiting the recruitment of CCR2Respiratory research · 2026Article
- HIV heart inflammation is mediated by HIV infected myeloid cells, HIV-tat secretion, and aberrant function of Connexin43-containing channels.Scientific reports · 2026Article
- Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Macrophage surface protein Mac-2 mediates inflammatory and stromal stress pathways in doxorubicin-induced cardiac injury.Cardio-oncology (London, England) · 2026Article
- From marrow memory to adverse ventricular remodeling: trained immunity after myocardial infarction.Frontiers in immunology · 2026Review
- Myeloid cell-specific β2-adrenergic receptor deletion improves early cardiac injury resolution via de-repression of Anxa1.Theranostics · 2026Article
- Cell-Free DNA Profiles End-Organ Injury and Predicts Outcomes in Advanced Heart Failure With Left Ventricular Assist Device Implantation.Circulation. Heart failure · 2026Observational
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- A Cross-Layer Inflammatory Signature Links Residual Inflammatory Risk to Heart Failure Risk in Metabolic Syndrome: Network Mapping and Brown Adipose Transcriptomic Support.Journal of inflammation research · 2026Article
223 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 2 countries.
Hendrik B SagerFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.). mnahrendorf@mgh.harvard.edu hendrik.sager@tum.de.
Maarten HulsmansFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Kory J LavineFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Marina B MoreiraFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Timo HeidtFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Gabriel CourtiesFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Yuan SunFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Yoshiko IwamotoFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Benoit TricotFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Omar F KhanFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
James E DahlmanFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Anna BorodovskyFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Kevin FitzgeraldFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Daniel G AndersonFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Ralph WeisslederFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Peter LibbyFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Filip K SwirskiFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).
Matthias NahrendorfFrom the Center for Systems Biology, Department of Imaging (H.B.S., M.H., T.H., G.C., Y.S., Y.I., B.T., R.W., F.K.S., M.N.) and Cardiovascular Research Center (M.N.), Massachusetts General Hospital and Harvard Medical School, Boston; Center for Cardiovascular Research, Washington University School of Medicine, St Louis, MS (K.J.L.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, MA (M.B.M., P.L.); Department of Cardiology and Angiology I, Heart Center Freiburg University, Germany (T.H.); Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA (O.F.K., J.E.D., D.G.A.); David H. Koch Institute for Integrative Cancer Research (O.F.K., J.E.D., D.G.A.) and Department of Chemical Engineering (D.G.A.), Massachusetts Institute of Technology, Cambridge; Alnylam Pharmaceuticals, Cambridge, MA (A.B., K.F.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.). mnahrendorf@mgh.harvard.edu hendrik.sager@tum.de.
Massachusetts Institute of Technology · USAlnylam Pharmaceuticals (United States) · USCenter for Systems Biology · USHarvard University · USHarvard–MIT Division of Health Sciences and Technology · USUniversity of Freiburg · DEWashington University in St. Louis · US
Funding
Monocyte Heterogeneity in Experimental and Human AtherosclerosisR01HL095612 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI SWIRSKI, FILIP K · 2009 to 2016
$3.4MLifestyle effects on hematopoiesis and atherosclerosisR01HL128264 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS, SWIRSKI, FILIP K · 2015 to 2018
$3.3MPET/MRI of cardiac repairR01HL096576 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2009 to 2017
$2.8MSingle Cell Imaging of the HeartR01HL122208 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI WEISSLEDER, MD, PHD, RALPH · 2014 to 2017
$1.7MCell-Cell Interaction in Heart FailureR01HL117829 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2014 to 2017
$1.7MEMBRYONIC-DERIVED MACROPHAGES IN CORONARY DEVELOPMENT AND ADULT CORONARY GROWTHK08HL123519 · NHLBI · WASHINGTON UNIVERSITY · PI LAVINE, KORY J. · 2014 to 2018
$715kNHLBI NIH HHS K08 HL123519NHLBI NIH HHS R01 HL095612NHLBI NIH HHS R01 HL096576NHLBI NIH HHS R01 HL117829NHLBI NIH HHS R01 HL122208NHLBI NIH HHS R01 HL128264
Abstract
rationaleMacrophages reside in the healthy myocardium, participate in ischemic heart disease, and modulate myocardial infarction (MI) healing. Their origin and roles in post-MI remodeling of nonischemic remote myocardium, however, remain unclear.
objectiveThis study investigated the number, origin, phenotype, and function of remote cardiac macrophages residing in the nonischemic myocardium in mice with chronic heart failure after coronary ligation. METHODS AND
resultsEight weeks post MI, fate mapping and flow cytometry revealed that a 2.9-fold increase in remote macrophages results from both increased local macrophage proliferation and monocyte recruitment. Heart failure produced by extensive MI, through activation of the sympathetic nervous system, expanded medullary and extramedullary hematopoiesis. Circulating Ly6C(high) monocytes rose from 64±5 to 108±9 per microliter of blood (P<0.05). Cardiac monocyte recruitment declined in Ccr2(-/-) mice, reducing macrophage numbers in the failing myocardium. Mechanical strain of primary murine and human macrophage cultures promoted cell cycle entry, suggesting that the increased wall tension in post-MI heart failure stimulates local macrophage proliferation. Strained cells activated the mitogen-activated protein kinase pathway, whereas specific inhibitors of this pathway reduced macrophage proliferation in strained cell cultures and in the failing myocardium (P<0.05). Steady-state cardiac macrophages, monocyte-derived macrophages, and locally sourced macrophages isolated from failing myocardium expressed different genes in a pattern distinct from the M1/M2 macrophage polarization paradigm. In vivo silencing of endothelial cell adhesion molecules curbed post-MI monocyte recruitment to the remote myocardium and preserved ejection fraction (27.4±2.4 versus 19.1±2%; P<0.05).
conclusionsMyocardial failure is influenced by an altered myeloid cell repertoire.
Indexed as
AnimalsBiomechanical PhenomenaCell ProliferationCells, CulturedChronic DiseaseFemaleHeart FailureHumansMacrophagesMaleMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicMyocardiumheart failurehypertrophymacrophagemonocytemyocardial infarction
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