ArticleThe Journal of experimental medicine2018
Cardiac macrophages promote diastolic dysfunction.
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Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 320 papers, 5 of them syntheses that pooled it.
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320citing papers in PubMed, 5 pooled it
31.6field-weighted citation impact, top 1% of its field
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Who cites it
320 citing papers in PubMed, 5 syntheses or guidelines pooled it, 488 citations in OpenAlex.
- Immunology of heart failure with preserved ejection fraction.Expert review of clinical immunology · 2025Pooled it
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- Association of systemic inflammatory markers with clinical adverse prognosis and outcomes in HFpEF: a systematic review and meta-analysis of cohort studies.Frontiers in cardiovascular medicine · 2024Pooled it
- Sex differences in pharmacological interventions and their effects on lifespan and healthspan outcomes: a systematic review.Frontiers in aging · 2023Pooled it
- Multifunctional biomaterial platforms for blocking the fibrosis process and promoting cellular restoring effects in myocardial fibrosis therapy.Frontiers in bioengineering and biotechnology · 2022Pooled it
- Neuromodulation of Inflammation to Treat Heart Failure With Preserved Ejection Fraction: A Pilot Randomized Clinical Trial.Journal of the American Heart Association · 2022Trial
- Bidirectional metabolic-vascular feedback loops in heart failure: From myocardial energetics to multisystem cardiometabolic crosstalk.iScience · 2026Review
- Myeloid Cell Expansion Propels Right Ventricular Dysfunction in HFpEF Through Sterile Inflammation.Circulation · 2026Article
- Candidate Residual Inflammatory Risk in HFpEF: A Multiorgan Framework for Longitudinal Phenotyping, Trial Enrichment, and Therapeutic Evidence Appraisal.Cardiovascular drugs and therapy · 2026Review
- Macrophage-Dependent Intercellular Crosstalk in Multiphenotypic Heart Failure With Preserved Ejection Fraction.Journal of the American Heart Association · 2026Review
- Single-Cell Analysis of Human Heart Failure With Preserved Ejection Fraction.Circulation research · 2026Article
- Inflammation, metabolism, and aging in heart failure with preserved ejection fraction: Mechanisms and treatment perspectives.Journal of translational internal medicine · 2026Article
- Immunometabolic Organ Crosstalk in Heart Failure with Preserved Ejection Fraction: The Role of Dietary Patterns in Obesity-Related Inflammation.Nutrients · 2026Review
- Integrated transcriptomic analysis reveals lymphaticZoological research · 2026Article
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- Oridonin as a novel KDM5C inhibitor alleviates clonal hematopoiesis-induced cardiac agingActa pharmaceutica Sinica. B · 2026Article
- The impact of inflammation, neuromodulation, and gut microbiota on developing cardiac fibrosis and hypertension.Cardiovascular research · 2026Review
- The interaction between microbes and cytokines in cancer: unraveling the underlying effects.Journal of translational medicine · 2026Review
- Macrophages of the heart: Homeostasis and disease.Biomedical journal · 2026Review
- Neuroimmune interactions in cardiovascular homeostasis and disease.American journal of physiology. Cell physiology · 2026Review
260 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 4 institutions in 1 country.
Maarten HulsmansCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-1009-658X
Hendrik B SagerCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Jason D RohCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
María Valero-MuñozWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA.ORCID 0000-0002-1412-7366
Nicholas E HoustisCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Yoshiko IwamotoCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Yuan SunCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Richard M WilsonWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA.
Gregory WojtkiewiczCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-3148-8411
Benoit TricotCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Michael T OsborneDivision of Cardiology and Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Judy HungDivision of Cardiology and Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Claudio VinegoniCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-9818-3639
Kamila NaxerovaCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
David E SosnovikCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Michael R ZileGazes Cardiac Research Institute, Medical University of South Carolina, Charleston, SC.
Amy D BradshawGazes Cardiac Research Institute, Medical University of South Carolina, Charleston, SC.
Ronglih LiaoDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Ahmed TawakolDivision of Cardiology and Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Ralph WeisslederCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Anthony RosenzweigCardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Filip K SwirskiCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-3163-9152
Flora SamWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA.
Matthias NahrendorfCenter for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA mnahrendorf@mgh.harvard.edu.ORCID 0000-0002-4021-1887
Harvard University · USBoston University · USBrigham and Women's Hospital · USMedical University of South Carolina · US
Funding
Harvard Clinical and Translational Science CenterKL2TR001100 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$8.5MCardiac MR and CT ResearchT32HL076136 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NEILAN, TOMAS G · 2004 to 2019
$4.9MPlasma miRNA predictors of adverse mechanical and electrical remodeling after MIUH3TR000901 · NCATS · MASSACHUSETTS GENERAL HOSPITAL · PI DAS, SAUMYA, KWONG, RAYMOND Y · 2015 to 2017
$3.2MPET/MRI of cardiac repairR01HL096576 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2009 to 2017
$2.8MInterfering with the macrophage life cycle of atherosclerosisR01HL125428 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ANDERSON, DANIEL G, NAHRENDORF, MATTHIAS · 2017 to 2020
$1.9MDoes Exercise Induce Cardiomyogenesis?R01HL122987 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ROSENZWEIG, ANTHONY · 2014 to 2018
$1.7MCell-Cell Interaction in Heart FailureR01HL117829 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2014 to 2017
$1.7MRole of miR-222 in pathological hypertrophy and heart failureR01HL135886 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ROSENZWEIG, ANTHONY · 2017 to 2020
$1.7MRole of Aldosterone and Adiponectin in Inter-Tissue Communication in Diastolic HeR01HL117153 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAM, FLORA · 2013 to 2016
$1.6MExtracellular Matrix in Hypertensive Heart Disease & Transition to Heart FailureR01HL123478 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ZILE, MICHAEL R · 2015 to 2018
$1.5MPlasma miRNA predictors of adverse mechanical and electrical remodeling after MIUH2TR000901 · NCATS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI DAS, SAUMYA, KWONG, RAYMOND Y · 2013 to 2014
$1.1MNCATS NIH HHS KL2 TR001100NCATS NIH HHS UH2 TR000901NCATS NIH HHS UH3 TR000901NHLBI NIH HHS R01 HL096576NHLBI NIH HHS R01 HL117153NHLBI NIH HHS R01 HL117829NHLBI NIH HHS R01 HL122987NHLBI NIH HHS R01 HL123478NHLBI NIH HHS R01 HL125428NHLBI NIH HHS R01 HL135886NHLBI NIH HHS T32 HL076136
Abstract
Macrophages populate the healthy myocardium and, depending on their phenotype, may contribute to tissue homeostasis or disease. Their origin and role in diastolic dysfunction, a hallmark of cardiac aging and heart failure with preserved ejection fraction, remain unclear. Here we show that cardiac macrophages expand in humans and mice with diastolic dysfunction, which in mice was induced by either hypertension or advanced age. A higher murine myocardial macrophage density results from monocyte recruitment and increased hematopoiesis in bone marrow and spleen. In humans, we observed a parallel constellation of hematopoietic activation: circulating myeloid cells are more frequent, and splenic
Indexed as
AdultAgedAgingAnimalsDiastoleFemaleFibroblastsHeartHeart FailureHematopoiesisHomeostasisHumansHypertensionInterleukin-10MacrophagesMaleIL10 protein, mouseInterleukin-10
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LicenceCC BY-NC-SA
Read underepoch 390
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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.