Notably, despite this overlap, direct experimental proof that SARS-CoV-2-evoked TLR signaling causally perturbs canonical PAH pathways (e.g., BMPR2) remains limited; conversely, TLR3 activation can upregulate BMPR2 and ameliorate experimental PH, whereas TLR4 is implicated in pulmonary vascular homeostasis and its loss favors remodeling—underscoring context dependence [19,22]. This evidence concerns the gene TLR3 and pulmonary arterial hypertension.