3.8 Review

Neutrophil roles in left ventricular remodeling following myocardial infarction

Journal

FIBROGENESIS & TISSUE REPAIR
Volume 6, Issue -, Pages -

Publisher

BMC
DOI: 10.1186/1755-1536-6-11

Keywords

PMNs; Myocardial infarction; Inflammation; Innate immunity; Degranulation; Matrix metalloproteinases

Categories

Funding

  1. NIH/NHLBI HHSN for the San Antonio Cardiovascular Proteomics Center [268201000036C, N01-HV00244, R01 HL075360]
  2. Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development [5I01BX000505]
  3. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL075360] Funding Source: NIH RePORTER
  4. Veterans Affairs [I01BX000505] Funding Source: NIH RePORTER

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Polymorphonuclear granulocytes (PMNs; neutrophils) serve as key effector cells in the innate immune system and provide the first line of defense against invading microorganisms. In addition to producing inflammatory cytokines and chemokines and undergoing a respiratory burst that stimulates the release of reactive oxygen species, PMNs also degranulate to release components that kill pathogens. Recently, neutrophil extracellular traps have been shown to be an alternative way to trap microorganisms and contain infection. PMN- derived granule components are also involved in multiple non-infectious inflammatory processes, including the response to myocardial infarction (MI). In this review, we will discuss the biological characteristics, recruitment, activation, and removal of PMNs, as well as the roles of PMN- derived granule proteins in inflammation and innate immunity, focusing on the MI setting when applicable. We also discuss future perspectives that will direct research in PMN biology.

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