ABSTRACT
Lung fibrosis is characterized by dysregulated wound healing with excessive scarring in the lung tissues, which results in organ failure. This fatal disease has no cure and has only limited treatment options. With its late age onset and environmental influences, it is regarded as a dysregulated epigenetic disease. Emerging data have shown that epigenetic mechanisms are involved in the disease pathogenesis. Epigenetic alterations, including DNA methylation, noncoding RNA, and histone modifications are all reported in this disease. There are cross-talks among different epigenetic modifications, as one alteration would affect other modifications and would change related gene expression. Histone modifications are critical regulators in gene transcription, which are reversible and plastic. Therefore, histone modifications are novel targets for developing new therapeutic options. This review focuses on the roles of histone modifications, mainly histone acetylation and methylation, as well as their related enzymes in the pathogenesis of lung fibrosis.
