By Dr Deepu
Researchers found in “both human cells and mice” that “exposure to silica dust may trigger pulmonary fibrosis (PF) because silica particles block a self-cleansing process used by cells, termed autophagy, which drives cell death in the lungs.”
The researchers have summarized their study by saying” we have shown that autophagy participates in SiNPs-induced PF. We have also identified that the autophagic flux blockage results from lysosomal acidification inhibition, which then triggers apoptosis in AECs and subsequent PF. These findings provide a new mechanism by which SiNPs trigger PF by targeting AECs. Furthermore, these results may lead to new strategies to prevent SiNPs-induced PF by enhancing autophagic degradation”.
The findings were published in Cell Death & Disease.
Researchers found in “both human cells and mice” that “exposure to silica dust may trigger pulmonary fibrosis (PF) because silica particles block a self-cleansing process used by cells, termed autophagy, which drives cell death in the lungs.”
The researchers have summarized their study by saying” we have shown that autophagy participates in SiNPs-induced PF. We have also identified that the autophagic flux blockage results from lysosomal acidification inhibition, which then triggers apoptosis in AECs and subsequent PF. These findings provide a new mechanism by which SiNPs trigger PF by targeting AECs. Furthermore, these results may lead to new strategies to prevent SiNPs-induced PF by enhancing autophagic degradation”.
The findings were published in Cell Death & Disease.
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