A narrative review: CXC chemokines influence immune surveillance in obesity and obesity-related diseases: Type 2 diabetes and nonalcoholic fatty liver disease.
CXC chemokines
Inflammation
Nonalcoholic fatty liver disease
Obesity
Therapeutic potential
Type 2 diabetes
Journal
Reviews in endocrine & metabolic disorders
ISSN: 1573-2606
Titre abrégé: Rev Endocr Metab Disord
Pays: Germany
ID NLM: 100940588
Informations de publication
Date de publication:
08 2023
08 2023
Historique:
accepted:
11
03
2023
medline:
8
8
2023
pubmed:
1
4
2023
entrez:
31
3
2023
Statut:
ppublish
Résumé
Adipose tissue develops lipids, aberrant adipokines, chemokines, and pro-inflammatory cytokines as a consequence of the low-grade systemic inflammation that characterizes obesity. This low-grade systemic inflammation can lead to insulin resistance (IR) and metabolic complications, such as type 2 diabetes (T2D) and nonalcoholic fatty liver disease (NAFLD). Although the CXC chemokines consists of numerous regulators of inflammation, cellular function, and cellular migration, it is still unknown that how CXC chemokines and chemokine receptors contribute to the development of metabolic diseases (such as T2D and NAFLD) during obesity. In light of recent research, the objective of this review is to provide an update on the linkage between the CXC chemokine, obesity, and obesity-related metabolic diseases (T2D and NAFLD). We explore the differential migratory and immunomodulatory potential of CXC chemokines and their mechanisms of action to better understand their role in clinical and laboratory contexts. Besides that, because CXC chemokine profiling is strongly linked to leukocyte recruitment, macrophage recruitment, and immunomodulatory potential, we hypothesize that it could be used to predict the therapeutic potential for obesity and obesity-related diseases (T2D and NAFLD).
Identifiants
pubmed: 37000372
doi: 10.1007/s11154-023-09800-w
pii: 10.1007/s11154-023-09800-w
pmc: PMC10063956
doi:
Substances chimiques
Chemokines, CXC
0
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
611-631Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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