Cited by 95Cardiac Fibrosis and RemodelingAtherosclerosis and Cardiovascular DiseasesCardiac Ischemia and Reperfusion

Innate immune cells in ischaemic heart disease: does myocardial infarction beget myocardial infarction?

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Nahrendorf, Matthias, Swirski, Filip K.·2016·European Heart Journal

Abstract

Knowledge of macrophages in steady-state and diseased tissue is rapidly expanding, propelled by improved diagnostic capacity to detect and monitor cells in their native environments. In this review, we discuss implications for ischaemic heart disease and examine innate immune cell pathways that increase systemic leucocyte supply after myocardial infarction (MI). Acute MI alters the macrophage phenotype and supply chain from tissue resident to blood monocytes sourced from haematopoietic organs. That blood leucocytosis closely associates with cardiovascular mortality provides a strong motivation to understand why and how organ ischaemia alters cellular immunity.

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Crossref · 10.1093/eurheartj/ehv453

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  • Cardiac macrophages may either tailor the delivery of iron to the myocardium or accumulate and detoxify heme which may mainly arise from tissue injury.

    “In addition, their roles in the metabolic activity of the adjacent myocardium and in chronic cardiac diseases such as congestive heart failure are increasingly appreciated [199], and macrophages may either tailor the delivery of iron to the myocardium or accumulate and detoxify heme which may mainly arise from tissue injury [161, 214].”

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Authors
Nahrendorf, M., & Swirski, F. K.
Affiliations
Harvard University (US)
Corresponding author
Nahrendorf, Matthias
Venue
European Heart Journal
Published
2015-09-08
Volume
37
Issue
11
Pages
868-872
ISSN
  • 0195-668X (ISSN-L)
  • 1522-9645
OpenAlex
W2128368961
Cited by
95
References
64
Citations by year
2026: 9 · 2025: 5 · 2024: 13 · 2023: 7 · 2022: 8 · 2021: 6 · 2020: 7 · 2019: 8 · 2018: 11 · 2017: 9 · 2016: 10 · 2015: 1
FWCI
1.77
Type
journal article
Language
en
Open access
Locations
  • European Heart Journal (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
  • National Institutes of Health (R01HL117829, R01NS084863)
  • MGH Research Scholar Award (R01HL095612, R56AI104695)
  • Howard M. Goodman Fellowship
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
Keywords
ischemic heart disease, myocardial infarction, innate immunity, macrophages, monocytes, leukocytosis, macrophage phenotype, cardiovascular mortality
MeSH terms
Bone Marrow Cells, Humans, Immunity, Innate, Life Style, Macrophages, Monocytes, Myocarditis, Phenotype, Spleen, Myocardial Ischemia, Cell Proliferation, Drug Discovery

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