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These activated Smads form a complex with Smad4, which translocates to the nucleus and promotes the expression of pro-fibrotic genes [24], such as Type I Collagen alpha 1 (COL1A1) and Fibronectin and Connective Tissue Growth Factor (CTGF)
Through oligomerization, ninjurin-1 causes the plasma membrane to rupture completely, resulting in the efflux of large damage-associated molecular patterns (161, 162)
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