The role of cigarette smoke-induced epigenetic alterations in inflammation
Abstract Background Exposure to cigarette smoke (CS) is a major threat to human health worldwide. It is well established that smoking increases the risk of respiratory diseases, cardiovascular diseases and different forms of cancer, including lung, liver, and colon. CS-triggered inflammation is cons...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2019-11-01
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| Series: | Epigenetics & Chromatin |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s13072-019-0311-8 |
| _version_ | 1818339842681995264 |
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| author | Dandan Zong Xiangming Liu Jinhua Li Ruoyun Ouyang Ping Chen |
| author_facet | Dandan Zong Xiangming Liu Jinhua Li Ruoyun Ouyang Ping Chen |
| author_sort | Dandan Zong |
| collection | DOAJ |
| description | Abstract Background Exposure to cigarette smoke (CS) is a major threat to human health worldwide. It is well established that smoking increases the risk of respiratory diseases, cardiovascular diseases and different forms of cancer, including lung, liver, and colon. CS-triggered inflammation is considered to play a central role in various pathologies by a mechanism that stimulates the release of pro-inflammatory cytokines. During this process, epigenetic alterations are known to play important roles in the specificity and duration of gene transcription. Main text Epigenetic alterations include three major modifications: DNA modifications via methylation; various posttranslational modifications of histones, namely, methylation, acetylation, phosphorylation, and ubiquitination; and non-coding RNA sequences. These modifications work in concert to regulate gene transcription in a heritable fashion. The enzymes that regulate these epigenetic modifications can be activated by smoking, which further mediates the expression of multiple inflammatory genes. In this review, we summarize the current knowledge on the epigenetic alterations triggered by CS and assess how such alterations may affect smoking-mediated inflammatory responses. Conclusion The recognition of the molecular mechanisms of the epigenetic changes in abnormal inflammation is expected to contribute to the understanding of the pathophysiology of CS-related diseases such that novel epigenetic therapies may be identified in the near future. |
| first_indexed | 2024-12-13T15:33:26Z |
| format | Article |
| id | doaj.art-1ec426f392ed4a16803c181ae3315f84 |
| institution | Directory Open Access Journal |
| issn | 1756-8935 |
| language | English |
| last_indexed | 2024-12-13T15:33:26Z |
| publishDate | 2019-11-01 |
| publisher | BMC |
| record_format | Article |
| series | Epigenetics & Chromatin |
| spelling | doaj.art-1ec426f392ed4a16803c181ae3315f842022-12-21T23:40:06ZengBMCEpigenetics & Chromatin1756-89352019-11-0112112510.1186/s13072-019-0311-8The role of cigarette smoke-induced epigenetic alterations in inflammationDandan Zong0Xiangming Liu1Jinhua Li2Ruoyun Ouyang3Ping Chen4Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South UniversityDepartment of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South UniversityDepartment of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South UniversityDepartment of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South UniversityDepartment of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South UniversityAbstract Background Exposure to cigarette smoke (CS) is a major threat to human health worldwide. It is well established that smoking increases the risk of respiratory diseases, cardiovascular diseases and different forms of cancer, including lung, liver, and colon. CS-triggered inflammation is considered to play a central role in various pathologies by a mechanism that stimulates the release of pro-inflammatory cytokines. During this process, epigenetic alterations are known to play important roles in the specificity and duration of gene transcription. Main text Epigenetic alterations include three major modifications: DNA modifications via methylation; various posttranslational modifications of histones, namely, methylation, acetylation, phosphorylation, and ubiquitination; and non-coding RNA sequences. These modifications work in concert to regulate gene transcription in a heritable fashion. The enzymes that regulate these epigenetic modifications can be activated by smoking, which further mediates the expression of multiple inflammatory genes. In this review, we summarize the current knowledge on the epigenetic alterations triggered by CS and assess how such alterations may affect smoking-mediated inflammatory responses. Conclusion The recognition of the molecular mechanisms of the epigenetic changes in abnormal inflammation is expected to contribute to the understanding of the pathophysiology of CS-related diseases such that novel epigenetic therapies may be identified in the near future.http://link.springer.com/article/10.1186/s13072-019-0311-8EpigeneticDNA methylationHistone modificationmiRNALncRNAInflammation |
| spellingShingle | Dandan Zong Xiangming Liu Jinhua Li Ruoyun Ouyang Ping Chen The role of cigarette smoke-induced epigenetic alterations in inflammation Epigenetics & Chromatin Epigenetic DNA methylation Histone modification miRNA LncRNA Inflammation |
| title | The role of cigarette smoke-induced epigenetic alterations in inflammation |
| title_full | The role of cigarette smoke-induced epigenetic alterations in inflammation |
| title_fullStr | The role of cigarette smoke-induced epigenetic alterations in inflammation |
| title_full_unstemmed | The role of cigarette smoke-induced epigenetic alterations in inflammation |
| title_short | The role of cigarette smoke-induced epigenetic alterations in inflammation |
| title_sort | role of cigarette smoke induced epigenetic alterations in inflammation |
| topic | Epigenetic DNA methylation Histone modification miRNA LncRNA Inflammation |
| url | http://link.springer.com/article/10.1186/s13072-019-0311-8 |
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