SAMP1/TMEM201 protects alveolar type 2 cells from DNA damage-associated senescence and restrains pulmonary fibrosis
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease in which repetitive injury to the alveolar epithelium and senescence of alveolar type 2 (AT2) cells drive persistent myofibroblast activation and extracellular matrix deposition. Inner nuclear membrane (INM) proteins organise nuclear architecture and participate in the DNA damage response, but whether they influence…
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by repeated injury to alveolar cells and their subsequent aging. Nuclear membrane proteins help maintain cell structure and respond to DNA damage, but their role in AT2 cell senescence and fibrosis is unclear. Researchers have discovered SAMP1/TMEM201, an INM protein that protects AT2 cells from DNA damage-induced aging.
In a model of pulmonary fibrosis, reducing SAMP1 in AT2 cells worsened fibrosis, while delivering SAMP1 before bleomycin exposure reduced both fibrosis and related gene expression. The data suggest that preserving SAMP1-AT2 interaction may be a potential therapeutic strategy for IPF, as it protects the epithelium from altered DNA damage signaling.
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