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The x-factor involved in apoptosis and proliferation—reciprocal exosome cross-talk between lymphangioleiomyomatosis-derived smooth muscle cells (LAM-SMCs) and endothelial cells (ECs) mediates EC network disruption/apoptosis and promotes LAM-SMC growth

      Introduction: Lymphangioleiomyomatosis (LAM) is a progressive and incurable disease caused by mutations in the TSC2 gene, which is involved in mTOR pathway regulation. Fragile endothelial cell (EC) neovessels are stabilized by mural smooth muscle cells (SMCs). However, SMC-like LAM cells invade and destroy the lung through unknown mechanism(s). We postulate that LAM-SMCs will disrupt EC capillary-like networks and promote EC apoptosis.
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