This review provides a focused synthesis of the hematologic and immunologic mechanisms shared by both conditions—such as cytokine overexpression (notably TGF-β, IL-6, and TNF-α), endothelial dysfunction, immune dysregulation, and microvascular thrombosis—and emphasizes how SARS-CoV-2 infection may act as a catalyst for accelerated fibrotic remodeling in IPF. Here, TGFB1 is linked to endothelial dysfunction.