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Together, these interconnected signaling cascades reshape transcriptional programs in fibroblasts, AECs, and endothelial cells, promoting myofibroblast differentiation, epithelial cell dysfunction, immune dysregulation, and excessive ECM deposition, which collectively drive the onset and progression of pulmonary fibrosis [33, 39] (Fig

To explore the lung regeneration process following successful fibrosis clearance, we mapped cellular profile by the scRNA-seq analysis of lungs between BLM+Saline and CD5/ LNP groups via the 10Genomics platform (Fig

Thymidine as a kinetic and biochemical modulator of 1-beta-D-arabinofuranosylcytosine in human acute nonlymphocytic leukemia

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