Pulmonary arterial hypertension (PAH) is a progressive disorder characterized by excessive remodeling of the distal vessels, resulting in increased pulmonary vascular resistance and subsequent right heart failure. Distinct subtypes of mural cells, notably smooth muscle cells (SMCs) and pericytes, have been implicated in disease progression in both animal models and human studies. Key histological features of the lungs from patients with PAH include an enhanced accumulation of SMCs within the distal arteries. Despite these findings, the precise molecular mechanisms and signaling pathways by which these cell types lead to vascular remodeling remain poorly defined. A deeper understanding of the pathogenic contributions of SMCs and pericytes is crucial for the development of effective disease-modifying therapies. In this chapter, we review and summarize the current literature on the role of SMCs and pericytes in PAH, highlighting critical molecular pathways such as the SDF-1/CXCR4 axis, TGF-β, and noncoding RNA families. Additionally, we address existing limitations and critical knowledge gaps in studying the specific contributions of these cells to pulmonary vascular remodeling.