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Immunometabolism and mitochondria in inflammatory bowel disease: a role for therapeutic intervention?
被引:0
|作者:
Adams, Claire E.
[1
]
Rutherford, Duncan G.
[1
]
Jones, Gareth R.
[1
]
Ho, Gwo-tzer
[1
]
机构:
[1] Univ Edinburgh, Inst Regenerat & Repair, Ctr Inflammat Res, Gut Res Unit, Edinburgh EH16 4UU, Scotland
基金:
英国惠康基金;
关键词:
SUCCINATE;
SIGNAL;
HOMEOSTASIS;
METABOLISM;
ACTIVATION;
ITACONATE;
NLRX1;
D O I:
10.1242/dmm.050895
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Inflammatory bowel diseases (IBDs), incurable conditions characterised by recurrent episodes of immune-mediated gut inflammation and damage of unknown aetiology, are common. Current advanced therapies target key leukocyte-trafficking and cytokine-signalling hubs but are only effective in 50% of patients. With growing evidence of mitochondrial dysfunction in IBD and advances in our understanding of the role of metabolism in inflammation, we provide an overview of novel metabolic approaches to IBD therapy, challenging the current 'therapeutic ceiling', identifying critical pathways for intervention and reimagining metabolic biomarkers for the 21st century.
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