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Abstract: Epigenetics is defined as a heritable change occurring in gene expression and phenotype without altering the underlying primary DNA sequence itself. Epigenetic variation consists of DNA methylation repatterning, posttranslational modification of histone proteins, and non-coding RNAs (ncRNAs). Epigenetic modifications are deeply involved in tumorigenesis and tumor development. Epigenetic abnormalities can be therapeutically reversed, and three families of epigenetic marks, including “readers”, “writers” and “erasers”, could be modulated by epi drugs. Over the past decade, ten small-molecule epi drugs (e.g., inhibitors of DNA methyltransferases and histone deacetylases) have been approved by FDA or CFDA for the treatment of different cancers. Epigenetics therapy has been most effective in oncology and has become an attractive area in cancer treatment. Pulmonary hypertension (PH) encompasses a set of multifactorial diseases of progressive cardiopulmonary disorder. WHO classifies PH into five groups based on similar pathophysiological mechanisms, clinical presentation, haemodynamic characteristics, therapeutic management, and underlying etiology. Since PH shows many similarities with cancer, such as proliferation, resistance to apoptosis, and dysregulation of tumor suppressor genes, the current epigenetics therapeutic strategies used in cancer might be considered for the treatment of PH. The role of epigenetics in the setting of PH is a fast-growing field of research. In this review, we have summarized the up-to-date articles on the role of epigenetic mechanisms in the context of PH. The aim of this review is to provide a comprehensive insight from the epigenetics perspective and introduce the potential role of approved epi drugs in PH treatment.