Involvement of Oxidative Stress in Protective Cardiac Functions of Calprotectin

Calprotectin (CLP) belonging to the S-100 protein family is a heterodimeric complex (S100A8/S100A9) formed by two binding proteins. Upon cell activation, CLP stored in neutrophils is released extracellularly in response to inflammatory stimuli and acts as damage-associated molecular patterns (DAMPs)...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2022-04, Vol.11 (7), p.1226
Main Authors: Rochette, Luc, Dogon, Geoffrey, Rigal, Eve, Zeller, Marianne, Cottin, Yves, Vergely, Catherine
Format: Article
Language:English
Subjects:
Alarmins
Alarmins - metabolism
Bacterial infections
Binding sites
Blood platelets
Calgranulin A
Calgranulin A - metabolism
Calgranulin B
Calgranulin B - metabolism
calprotectin
Cardiology and cardiovascular system
Cell activation
Glycosylation
Heart attacks
Homeostasis
Human health and pathology
Humans
Infections
Inflammation
Inflammation - metabolism
Kinases
Leukocyte L1 Antigen Complex
Leukocyte L1 Antigen Complex - metabolism
Leukocytes (neutrophilic)
Life Sciences
Localization
Molecular weight
Myocardium
Neutrophils
Oxidants
Oxidative Stress
Pathogens
Proteins
Review
S100 protein
S100 Proteins
S100 Proteins - metabolism
Therapeutic targets
TLR4 protein
Toll-like receptors
Tumor necrosis factor-TNF
Zinc
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Summary:Calprotectin (CLP) belonging to the S-100 protein family is a heterodimeric complex (S100A8/S100A9) formed by two binding proteins. Upon cell activation, CLP stored in neutrophils is released extracellularly in response to inflammatory stimuli and acts as damage-associated molecular patterns (DAMPs). S100A8 and S100A9 possess both anti-inflammatory and anti-bacterial properties. The complex is a ligand of the toll-like receptor 4 (TLR4) and receptor for advanced glycation end (RAGE). At sites of infection and inflammation, CLP is a target for oxidation due to its co-localization with neutrophil-derived oxidants. In the heart, oxidative stress (OS) responses and S100 proteins are closely related and intimately linked through pathophysiological processes. Our review summarizes the roles of S100A8, S100A9 and CLP in the inflammation in relationship with vascular OS, and we examine the importance of CLP for the mechanisms driving in the protection of myocardium. Recent evidence interpreting CLP as a critical modulator during the inflammatory response has identified this alarmin as an interesting drug target.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells11071226