These will make the cartilage formation of vascular SMC transdifferentiate, leading to vascular calcification.408 The expression of TLR3 is reduced in the lung tissue and endothelial cells of patients with pulmonary hypertension, and its deficiency increases the susceptibility to apoptosis and pulmonary hypertension.409 In addition to TLRs, the lack of NOD1 and NOD2 can lead to lipid deposition of atherosclerotic plaques and the reduction of inflammatory cell infiltration, so it has been identified as pre-disease factors.410. This evidence concerns the gene NOD1 and pulmonary arterial hypertension.