Mesangial Cells in Lupus Nephritis.
Cytokines
Growth factors
Lupus nephritis
Mesangial cells
Pathogenic signaling
miRNA
Journal
Current rheumatology reports
ISSN: 1534-6307
Titre abrégé: Curr Rheumatol Rep
Pays: United States
ID NLM: 100888970
Informations de publication
Date de publication:
05 01 2022
05 01 2022
Historique:
accepted:
26
10
2021
entrez:
5
1
2022
pubmed:
6
1
2022
medline:
27
1
2022
Statut:
epublish
Résumé
Mesangial cells are critical for the proper function of the glomerulus, playing roles in structural support and injury repair. However, they are also early responders to glomerular immune complex deposition and contribute to inflammation and fibrosis in lupus nephritis. This review highlights recent studies identifying signaling pathways and mediators in mesangial cell response to lupus-relevant stimuli. Anti-dsDNA antibodies, serum, or plasma from individuals with lupus nephritis, or specific pathologic factors activated multiple signaling pathways. These pathways largely included JAK/STAT/SOCS, PI3K/AKT, and MAPK and led to induction of proliferation and expression of multiple proinflammatory cytokines, growth factors, and profibrotic factors. NFκB activation was a common mediator of response. Mesangial cells proliferate and express a wide array of proinflammatory/profibrotic factors in response to a variety of lupus-relevant pathologic stimuli. While some of the responses are similar, the mechanisms involved appear to be diverse depending on the stimulus. Future studies are needed to fully elucidate these mechanisms with respect to the diverse milieu of stimuli.
Identifiants
pubmed: 34985599
doi: 10.1007/s11926-021-01048-0
pii: 10.1007/s11926-021-01048-0
doi:
Substances chimiques
Antibodies, Antinuclear
0
anti-dsDNA autoantibody
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
83Subventions
Organisme : U.S. Department of Defense
ID : W81XWH-16-1-0640
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.