Acute respiratory distress syndrome FXR/Sptlc2 signaling promotes alveolar macrophage mitophagy and limits lung inflammation.

FXR (Nr1h4) activation in alveolar macrophages enhances mitophagy via Sptlc2, reducing oxidative stress and inflammatory mediator production during acute respiratory distress syndrome.

• Why it matters: Mitophagy is essential for mitochondrial quality control, but its role in macrophage functional reprogramming during ARDS is unclear.
• What they did: The study identified Nr1h4 (FXR) as a transcriptional regulator of mitophagy in alveolar macrophages and showed FXR activation upregulates Sptlc2 to enhance mitophagy under inflammatory conditions.
• The result: FXR deficiency impairs mitophagy and exacerbates pulmonary inflammation and lung injury in vivo, establishing the FXR/Sptlc2 axis as a potential therapeutic target in ARDS.

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