Mechanism of macrophage mitochondrial transfer in CBNPs induced EndMT of pulmonary microvascular endothelial cells - PubMed
3 days ago
- #Endothelial-mesenchymal transition
- #Carbon black nanoparticles
- #Pulmonary fibrosis
- CBNPs exposure leads to impaired pulmonary function, collagen deposition, and EndMT activation.
- CBNPs suppress the PINK1/Parkin mitophagy pathway, causing PANoptosis in alveolar macrophages (AMs).
- Damaged mitochondria from AMs are transferred to pulmonary microvascular endothelial cells (MPVECs), inducing EndMT.
- IFI27 is identified as a key regulator of PANoptosis, binding to PINK1 and worsening mitochondrial dysfunction.
- Silencing IFI27 reduces PANoptosis and mitochondrial transfer, reversing EndMT in MPVECs.
- The IFI27-PINK1 axis is crucial in mitochondrial transfer, presenting a therapeutic target for CBNPs-induced pulmonary fibrosis.