Pulmonary hypertension (PH) is a progressive pulmonary vascular disease with a poor prognosis and limited treatment options. Emerging evidence suggests that metabolic reprogramming plays a central role in driving PH pathogenesis. Among the key metabolic factors, lactate-the end product of glycolysis-has gained increasing recognition as a crucial regulator linking cellular metabolism to functional activity. Additionally, lactylation, a newly identified post-translational modification associated with lactate metabolism, has been shown to influence protein function and gene expression, further implicating its role in PH. While previous reviews have introduced these concepts, a systematic framework that directly integrates these molecular mechanisms into the core pathological hallmarks of the disease has been notably absent. In this review, we systematically examine the potential molecular mechanisms by which lactate and lactylation contribute to PH pathogenesis. Specifically, we systematically dissect the multifaceted roles of lactate and lactylation through the lens of five distinct pathological pillars of PH: (1) aberrant proliferation of pulmonary artery smooth muscle cells (PASMCs), (2) dysregulated immune-inflammatory responses, (3) progressive pulmonary fibrosis, (4) abnormal vasoconstriction, and (5) PASMC ferroptosis. By structuring our analysis around these core processes, we offer a novel, integrated perspective on how a single metabolic axis-lactate and lactylation-concertedly drives the complex pathophysiology of PH. This review aims to provide a comprehensive and forward-looking perspective that may guide future research into PH pathophysiology and treatment.