TY - JOUR
T1 - Neutrophil crosstalk during cardiac wound healing after myocardial infarction
AU - Chalise, Upendra
AU - Becirovic-Agic, Mediha
AU - Lindsey, Merry L.
N1 - Funding Information:
D. Lindsey is a Stokes-Shackleford Professor at UNMC. We acknowledge funding from the N ational Institutes of Health under award numbers U54GM115458 and HL137319, the B iomedical Laboratory Research and Development Service of the VA Office of Research and Development under award number 5I01BX000505, and the S wedish Society for Medical Research under award number P19-0144. The content is solely the responsibility of the authors and does not necessarily represent the official views of any of the funding agencies. All authors have reviewed and approved the article.
Funding Information:
D. Lindsey is a Stokes-Shackleford Professor at UNMC. We acknowledge funding from the National Institutes of Healthunder award numbers U54GM115458 and HL137319, the Biomedical Laboratory Research and Development Service of the VA Office of Research and Developmentunder award number 5I01BX000505, and the Swedish Society for Medical Researchunder award number P19-0144. The content is solely the responsibility of the authors and does not necessarily represent the official views of any of the funding agencies. All authors have reviewed and approved the article.
Publisher Copyright:
© 2022 The Author(s)
PY - 2021/12
Y1 - 2021/12
N2 - Myocardial infarction (MI) initiates an intense inflammatory response that induces neutrophil infiltration into the infarct region. Neutrophils commence the pro-inflammatory response that includes upregulation of cytokines and chemokines (e.g. interleukin-1 beta) and degranulation of pre-formed proteases (e.g. matrix metalloproteinases-8 and matrix metalloproteinases-9) that degrade existing extracellular matrix to clear necrotic tissue. An increase or complete depletion of neutrophils both paradoxically impair MI resolution, indicating a complex role of neutrophils in cardiac wound healing. Following pro-inflammation, the neutrophil shifts to a reparative phenotype that promotes inflammation resolution and aids in scar formation. Across the shifts in phenotype, the neutrophil communicates with other cells to coordinate repair and scar formation. This review summarizes our current understanding of neutrophil crosstalk with cardiomyocytes and macrophages during MI wound healing.
AB - Myocardial infarction (MI) initiates an intense inflammatory response that induces neutrophil infiltration into the infarct region. Neutrophils commence the pro-inflammatory response that includes upregulation of cytokines and chemokines (e.g. interleukin-1 beta) and degranulation of pre-formed proteases (e.g. matrix metalloproteinases-8 and matrix metalloproteinases-9) that degrade existing extracellular matrix to clear necrotic tissue. An increase or complete depletion of neutrophils both paradoxically impair MI resolution, indicating a complex role of neutrophils in cardiac wound healing. Following pro-inflammation, the neutrophil shifts to a reparative phenotype that promotes inflammation resolution and aids in scar formation. Across the shifts in phenotype, the neutrophil communicates with other cells to coordinate repair and scar formation. This review summarizes our current understanding of neutrophil crosstalk with cardiomyocytes and macrophages during MI wound healing.
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U2 - 10.1016/j.cophys.2022.100485
DO - 10.1016/j.cophys.2022.100485
M3 - Review article
C2 - 35664861
AN - SCOPUS:85125468899
SN - 2468-8681
VL - 24
JO - Current Opinion in Physiology
JF - Current Opinion in Physiology
M1 - 100485
ER -