IL33/ST2 Axis in Diabetic Kidney Disease: A Literature Review.
IL-33
ST2
alarmin
chronic kidney disease
diabetes mellitus
renal disease
Journal
Medicina (Kaunas, Lithuania)
ISSN: 1648-9144
Titre abrégé: Medicina (Kaunas)
Pays: Switzerland
ID NLM: 9425208
Informations de publication
Date de publication:
14 Feb 2019
14 Feb 2019
Historique:
received:
10
12
2018
revised:
11
02
2019
accepted:
12
02
2019
entrez:
17
2
2019
pubmed:
17
2
2019
medline:
15
6
2019
Statut:
epublish
Résumé
Interleukin-33 (IL-33) is a cytokine belonging to the IL-1 family, playing a role in inflammatory, infectious and autoimmune diseases and expressed in the cellular nucleus in several tissues. High levels of IL-33 are expressed in epithelial barrier tissues and endothelial barriers. ST2 is a receptor for IL-33, expressed selectively on a subset of Th2 cells, mediating some of their functions. The IL-33/ST2 axis plays an important role in several acute and chronic inflammatory diseases, including asthma and rheumatoid arthritis. Different disorders are related to the activity of IL-33, ST2, or their axis, including cardiovascular disease or renal disturbances. Therefore, in the present work, a literature review was conducted, covering the period from 1 January 2000 to 30 November 2018, in PubMed, ScienceDirect, and Google Scholar database, to assess the involvement of the IL-33/ST2 axis in diabetic kidney disease. 6 articles directly dealing with the argument were identified, highlighting a clear link between IL-33/ST2 axis and diabetic kidney disease or related nephropathy. Overall, the involvement of ST2 seems to be more predictive than IL-33, especially in investigating the deterioration of kidney function; however, both compounds are pivotal in the field of renal diseases. Future studies are required to confirm the scientific evidences on larger and more heterogeneous cohorts.
Identifiants
pubmed: 30769901
pii: medicina55020050
doi: 10.3390/medicina55020050
pmc: PMC6410122
pii:
doi:
Substances chimiques
IL1RL1 protein, human
0
IL33 protein, human
0
Interleukin-1 Receptor-Like 1 Protein
0
Interleukin-33
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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