Molecular and Genetic Medicine

ISSN: 1747-0862

Open Access

Short Notes on DNA Methylation and Importance of Precision Medicine for Idiopathic Pulmonary Fibrosis


Gilbert Tortora*

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease with unknown etiology that leads to the formation of scar tissue in the lungs. Although the molecular mechanisms underlying IPF remain unclear, epigenetic changes have been implicated in the disease pathogenesis. Epigenetics refers to modifications to DNA and histones that alter gene expression without changing the DNA sequence itself. These modifications include DNA methylation, histone modifications, and non-coding RNA expression, all of which are influenced by environmental factors. Epigenetic changes have been observed in IPF, particularly alterations in DNA methylation and histone modifications. Studies have identified DNA methylation changes in genes related to extracellular matrix remodeling, inflammation, and oxidative stress, which are all pathways that are dysregulated in IPF.In addition, histone modifications, such as histone acetylation and methylation, have been shown to regulate the expression of genes involved in fibrosis and inflammation. Given the potential role of epigenetic changes in IPF, precision medicine approaches targeting epigenetic modifications have been proposed as a potential therapeutic strategy. One approach is the use of drugs that target specific epigenetic enzymes, such as histone deacetylases (HDACs) and DNA methyltransferases (DNMTs), which are involved in histone and DNA modifications, respectively. For example, HDAC inhibitors have been shown to reduce fibrosis and improve lung function in animal models of IPF. However, the use of these drugs in human clinical trials has been limited due to their potential side effects and lack of specificity


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