Role of Neutrophils in Cardiac Injury and Repair Following Myocardial Infarction.

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  • Author(s): Ma Y;Ma Y
  • Source:
    Cells [Cells] 2021 Jul 02; Vol. 10 (7). Date of Electronic Publication: 2021 Jul 02.
  • Publication Type:
    Journal Article; Review
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
    • Publication Information:
      Original Publication: Basel, Switzerland : MDPI
    • Subject Terms:
    • Abstract:
      Neutrophils are first-line responders of the innate immune system. Following myocardial infarction (MI), neutrophils are quickly recruited to the ischemic region, where they initiate the inflammatory response, aiming at cleaning up dead cell debris. However, excessive accumulation and/or delayed removal of neutrophils are deleterious. Neutrophils can promote myocardial injury by releasing reactive oxygen species, granular components, and pro-inflammatory mediators. More recent studies have revealed that neutrophils are able to form extracellular traps (NETs) and produce extracellular vesicles (EVs) to aggravate inflammation and cardiac injury. On the contrary, there is growing evidence showing that neutrophils also exert anti-inflammatory, pro-angiogenic, and pro-reparative effects, thus facilitating inflammation resolution and cardiac repair. In this review, we summarize the current knowledge on neutrophils' detrimental roles, highlighting the role of recently recognized NETs and EVs, followed by a discussion of their beneficial effects and molecular mechanisms in post-MI cardiac remodeling. In addition, emerging concepts about neutrophil diversity and their modulation of adaptive immunity are discussed.
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    • Contributed Indexing:
      Keywords: adaptive immunity; angiogenesis; cardiac remodeling; inflammation; macrophage; myocardial infarction; neutrophil
    • Accession Number:
      0 (Cytokines)
      0 (Inflammation Mediators)
      0 (Reactive Oxygen Species)
    • Publication Date:
      Date Created: 20210807 Date Completed: 20211026 Latest Revision: 20211026
    • Publication Date:
      20221213
    • Accession Number:
      PMC8305164
    • Accession Number:
      10.3390/cells10071676
    • Accession Number:
      34359844