In vivo studies showed Trem2+ macrophages decrease lipid accumulation and ferroptosis in diabetic nephropathy, indicating a protective role against IL-1β-mediated effects.
Key Points
Trem2+ macrophages alleviate lipid accumulation and ferroptosis in tubular cells, demonstrating their protective role in diabetic nephropathy.
Trem2 deficiency in macrophages led to increased IL-1β production and CD36 expression, which are linked to enhanced ferroptosis in renal cells.
Functional enrichment analysis revealed Trem2+ macrophages positively regulate metabolic processes and phagocytosis during diabetic nephropathy.
Inhibition of NF-κB prevented IL-1β-induced production of CD36, highlighting a key mechanism in macrophage involvement in diabetic nephropathy.