Heme oxygenase‑1 (HO‑1) is an inducible cytoprotective enzyme that degrades heme into free iron, carbon monoxide and biliverdin, which is then rapidly converted into bilirubin. These degradation products serve an important role in the regulation of inflammation, oxidative stress and apoptosis. While the expression level of HO‑1 is typically low in most cells, it may be highly expressed when induced by a variety of stimulating factors, a process that contributes to the regulation of cell homeostasis. In the 5'‑non‑coding region of the HO‑1 gene, there are two polymorphic sites, namely the (GT)n dinucleotide and T(‑413)A single nucleotide polymorphism sites, which regulate the transcriptional activity of HO‑1. These polymorphisms have been shown to be closely associated with the occurrence and progression of numerous diseases, including cardiovascular, pulmonary, liver and kidney, various types of cancer and viral diseases. The present article reviews the progress that has been made in research on the association between the two types of polymorphisms and these diseases, which is expected to provide novel strategies for the diagnosis, treatment and prognosis of various diseases.
Keywords: (GT)n dinucleotide polymorphism; HO‑1; T(‑413)A single nucleotide polymorphism; diseases; promoter polymorphism.