Indirect regulation of HMGB1 release by gasdermin D
Descripción general
Resumen del artículo
This study found that HMGB1 release from macrophages following inflammasome activation isn't through GSDMD pores as previously thought, but rather due to cell lysis. In an endotoxemia mouse model, HMGB1 release was independent of GSDMD, suggesting different pathways for these molecules in vivo.
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Scientists thought a tiny door let a special signal out of cells. But they found the cell actually bursts open to release the signal, like a balloon popping! This happens in our bodies too.
Posibles conflictos de intereses
None identified
Limitaciones identificadas
Explicación de la calificación
This study offers valuable insights into the mechanism of HMGB1 release, challenging the prevailing view of its dependence on GSDMD pores. The experiments are well-designed and the conclusions are supported by the data. However, the limitations regarding in vivo validation and potential off-target effects prevent a rating of 5.
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