Limiting mitochondrial stress during infection
Inflammatory responses by macrophages during infection are dynamically regulated but mechanism of regulation is not clearly understood.
The researchers show that inflammatory macrophages upregulate the transcription factor nuclear factor erythroid 2-like 1 (NRF1) to enhance flux through the ubiquitin proteasome system (UPS) and turn over mitochondrial proteins.
Such protein turnover limits mitochondrial stress, which otherwise engages the integrated stress response to augment inflammation.
https://www.cell.com/cell-reports/fulltext/S2211-1247(24)01131-8
