Vasculitis & polymyalgia rheumatica
FTY720 ameliorates experimental MPO-ANCA-associated vasculitis by regulating fatty acid oxidation via the neutrophil PPARα–CPT1a pathway
Authors' conclusion
FTY720 attenuated renal injury in EAV through upregulating FAO via the PPARα-CPT1a pathway in neutrophils
Study context
- Population
- Rats with experimental autoimmune vasculitis (EAV); neutrophils from patients with active ANCA-associated vasculitis (AAV) and normal controls; differentiated HL-60 cells
- Comparison
- FTY720 treatment in EAV and in anti-neutrophil cytoplasmic antibody (ANCA)-stimulated neutrophils
Methodological detailsexperimental autoimmune vasculitis model, RNA sequencing, in vitro neutrophil and HL-60 experiments
- Experimental autoimmune vasculitis model
- RNA sequencing
- In vitro neutrophil and HL-60 experiments
Main finding
As reported in the abstract
- FTY720 significantly attenuated renal injury and pulmonary haemorrhage in EAV
- Renal cortex RNA sequencing: enhanced fatty acid oxidation (FAO) and peroxisome proliferator-activated receptor (PPAR) signalling in FTY720-treated rats
- Decreased FAO in neutrophils of patients with active AAV vs normal controls
- FTY720-treated differentiated HL-60 cells: increased CPT1a and PPARα expression
- Blocking or knockdown of CPT1a or PPARα reversed FTY720's inhibition of ANCA-induced neutrophil respiratory burst and NETosis
Original publication
FTY720 ameliorates experimental MPO-ANCA-associated vasculitis by regulating fatty acid oxidation via the neutrophil PPARα–CPT1a pathway. Rheumatology (Oxford). Published 5 June 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →