Abstract
Pulmonary fibrosis is a condition defined as a recurrent and progressive interstitial fibrotic disease and is considered to be terminated by interstitial lung disease disorders. Accumulating evidence indicates that epigenetic alterations, including histone acetylation, play a pivotal role in this process. Histone acetylation is governed by histone acetyltransferases (HATs) and histone deacetylases (HDACs). Vorinostat is a member of a larger class of compounds that inhibit histone deacetylases. Even though the pathogenesis of lung fibrosis is complicated, hypotheses have been proposed in recent years that include inflammation, epithelial degradation, differentiated fibroblast, angiogenesis, and oxidative stress. Emerging evidence from several preclinical studies has shown that Vorinostat has beneficial effects in preventing or reversing fibrogenesis. In this review, we summarize the latest findings of the roles of HDACs in the pathogenesis of pulmonary fibrosis and highlight the potential antifibrotic mechanism of Vorinostat in this diseases.
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