Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases
Histone deacetylases (HDACs) are essential enzymes that play a pivotal role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl groups from histone and non-histone proteins. This deacetylation is a crucial post-translational modification that influences several cellul...
Uloženo v:
| Vydáno v: | BMB reports Ročník 58; číslo 8; s. 313 - 324 |
|---|---|
| Hlavní autoři: | , , , |
| Médium: | Journal Article |
| Jazyk: | korejština |
| Vydáno: |
생화학분자생물학회
31.08.2025
|
| Témata: | |
| ISSN: | 1976-6696, 1976-670X |
| On-line přístup: | Získat plný text |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | Histone deacetylases (HDACs) are essential enzymes that play a pivotal role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl groups from histone and non-histone proteins. This deacetylation is a crucial post-translational modification that influences several cellular processes, such as chromatin remodeling, transcriptional repression, and signal transduction. Recent studies have illuminated the significant involvement of HDACs in the pathogenesis of fibrotic diseases, conditions characterized by the excessive accumulation of extracellular matrix components leading to progressive organ dysfunction and failure. These diseases commonly affect the liver, kidney, heart, lung, and colon. The contribution of HDACs to fibrogenesis is multifaceted, involving the modulation of gene expression that governs inflammatory and fibrotic signaling pathways. Therefore, targeting HDACs with specific inhibitors has emerged as a promising therapeutic strategy to mitigate fibrosis in various organs. HDAC inhibitors (HDACi) can potentially reverse the aberrant gene expression profiles associated with fibrotic diseases by restoring acetylation levels, thus attenuating fibrotic responses. Several HDAC inhibitors, such as vorinostat, trichostatin A, and romidepsin, have shown efficacy in preclinical models of fibrosis, demonstrating their potential to suppress fibrogenic signaling pathways and reduce extracellular matrix deposition. In this review, we provide a comprehensive analysis of the current understanding of the roles of HDACs in the regulation of histone and non-histone proteins, and their implications for fibrotic diseases. We compare the molecular mechanisms by which different classes of HDACs contribute to fibrosis in various organs, and highlight the therapeutic potential of HDAC inhibition. This review underscores the importance of further research into HDAC-specific inhibitors as viable treatments for fibrotic diseases, aiming to develop targeted therapies that can effectively ameliorate fibrosis and improve patient outcomes. [BMB Reports 2025; 58(8): 313-324] |
|---|---|
| AbstractList | Histone deacetylases (HDACs) are essential enzymes that play a pivotal role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl groups from histone and non-histone proteins. This deacetylation is a crucial post-translational modification that influences several cellular processes, such as chromatin remodeling, transcriptional repression, and signal transduction. Recent studies have illuminated the significant involvement of HDACs in the pathogenesis of fibrotic diseases, conditions characterized by the excessive accumulation of extracellular matrix components leading to progressive organ dysfunction and failure. These diseases commonly affect the liver, kidney, heart, lung, and colon. The contribution of HDACs to fibrogenesis is multifaceted, involving the modulation of gene expression that governs inflammatory and fibrotic signaling pathways. Therefore, targeting HDACs with specific inhibitors has emerged as a promising therapeutic strategy to mitigate fibrosis in various organs. HDAC inhibitors (HDACi) can potentially reverse the aberrant gene expression profiles associated with fibrotic diseases by restoring acetylation levels, thus attenuating fibrotic responses. Several HDAC inhibitors, such as vorinostat, trichostatin A, and romidepsin, have shown efficacy in preclinical models of fibrosis, demonstrating their potential to suppress fibrogenic signaling pathways and reduce extracellular matrix deposition. In this review, we provide a comprehensive analysis of the current understanding of the roles of HDACs in the regulation of histone and non-histone proteins, and their implications for fibrotic diseases. We compare the molecular mechanisms by which different classes of HDACs contribute to fibrosis in various organs, and highlight the therapeutic potential of HDAC inhibition. This review underscores the importance of further research into HDAC-specific inhibitors as viable treatments for fibrotic diseases, aiming to develop targeted therapies that can effectively ameliorate fibrosis and improve patient outcomes. [BMB Reports 2025; 58(8): 313-324] Histone deacetylases (HDACs) are essential enzymes that play a pivotal role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl groups from histone and non-histone proteins. This deacetylation is a crucial post-translational modification that influences several cellular processes, such as chromatin remodeling, transcriptional repression, and signal transduction. Recent studies have illuminated the significant involvement of HDACs in the pathogenesis of fibrotic diseases, conditions characterized by the excessive accumulation of extracellular matrix components leading to progressive organ dysfunction and failure. These diseases commonly affect the liver, kidney, heart, lung, and colon. The contribution of HDACs to fibrogenesis is multifaceted, involving the modulation of gene expression that governs inflammatory and fibrotic signaling pathways. Therefore, targeting HDACs with specific inhibitors has emerged as a promising therapeutic strategy to mitigate fibrosis in various organs. HDAC inhibitors (HDACi) can potentially reverse the aberrant gene expression profiles associated with fibrotic diseases by restoring acetylation levels, thus attenuating fibrotic responses. Several HDAC inhibitors, such as vorinostat, trichostatin A, and romidepsin, have shown efficacy in preclinical models of fibrosis, demonstrating their potential to suppress fibrogenic signaling pathways and reduce extracellular matrix deposition. In this review, we provide a comprehensive analysis of the current understanding of the roles of HDACs in the regulation of histone and non-histone proteins, and their implications for fibrotic diseases. We compare the molecular mechanisms by which different classes of HDACs contribute to fibrosis in various organs, and highlight the therapeutic potential of HDAC inhibition. This review underscores the importance of further research into HDAC-specific inhibitors as viable treatments for fibrotic diseases, aiming to develop targeted therapies that can effectively ameliorate fibrosis and improve patient outcomes. |
| Author | Kyung Hyun Yoo Jong Hoon Park Nayun Choi Sunyoung Jang |
| Author_xml | – sequence: 2 fullname: Sunyoung Jang – sequence: 3 – sequence: 4 fullname: Nayun Choi – sequence: 5 fullname: Jong Hoon Park – sequence: 6 fullname: Kyung Hyun Yoo |
| BookMark | eNpdkDtPwzAUhS1UJErpjsTiBQmGFMd2_GBrw5uiSqgDW2QnNrWaOlGcDv0D_G7MowxM917d8517dI_BwDfeAHCaoklGBbmavcxeTTvBCNMEpRgfgGEqOUsYR2-Dfc8kOwLjEJxGlHKScomG4CNvfN85ve1d42Fj4cqFPprDyqjS9LtaBRPgxcPNNA-XsG9gvzKwM-_bWv0nlK9gzJXs57ZreuN8uIZu09au_AYCtE0HrdNx6UpYuWC-LpyAQ6vqYMa_dQSWd7fL_CGZL-4f8-k8WWdIJKXQKakk1TTTvOQGYYUM0YJTlXLGSqqtVZhwRpiwEhEqKOOWcSmxFliUZATOf2zXMaMrfBXq4mn6vIiPyzCLGCI8wyLqzv50oWg7t1HdrqCpRBQR8gkRCm-c |
| ContentType | Journal Article |
| DBID | HZB Q5X JDI |
| DEWEY | 572 |
| DOI | 10.5483/BMBRep.2024-0122 |
| DatabaseName | Korea Information Science Society (KISS) Korean Studies Information Service System (KISS) B-Type KoreaScience |
| DatabaseTitleList | |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Chemistry Anatomy & Physiology |
| DocumentTitleAlternate | Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases |
| EISSN | 1976-670X |
| EndPage | 324 |
| ExternalDocumentID | JAKO202526636037528 4190403 |
| GroupedDBID | --- 23N 2WC 5GY 5VS 85H 87B 9ZL AAFWJ ACGFO ACYCR ADBBV AENEX AFPKN ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BCNDV DIK E3Z F5P GROUPED_DOAJ GX1 HH5 HYE HZB JDI KQ8 OVT Q5X RNS RPM TR2 53G IPNFZ RIG |
| ID | FETCH-LOGICAL-k508-c8b13d94b45b7c7e02a0e3b874a1766c4bffa2376368f90348467f67992b828c3 |
| ISSN | 1976-6696 |
| IngestDate | Wed Oct 08 04:37:48 EDT 2025 Tue Oct 14 02:10:44 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 8 |
| Keywords | Histone deacetylase Non-histone deacetylase Therapeutic target Fibrosis HDAC |
| Language | Korean |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-k508-c8b13d94b45b7c7e02a0e3b874a1766c4bffa2376368f90348467f67992b828c3 |
| Notes | Korean Society for Biochemistry and Molecular Biology KISTI1.1003/JNL.JAKO202526636037528 |
| OpenAccessLink | http://click.ndsl.kr/servlet/LinkingDetailView?cn=JAKO202526636037528&dbt=JAKO&org_code=O481&site_code=SS1481&service_code=01 |
| PageCount | 12 |
| ParticipantIDs | kisti_ndsl_JAKO202526636037528 kiss_primary_4190403 |
| PublicationCentury | 2000 |
| PublicationDate | 20250831 |
| PublicationDateYYYYMMDD | 2025-08-31 |
| PublicationDate_xml | – month: 08 year: 2025 text: 20250831 day: 31 |
| PublicationDecade | 2020 |
| PublicationTitle | BMB reports |
| PublicationTitleAlternate | BMB Reports |
| PublicationYear | 2025 |
| Publisher | 생화학분자생물학회 |
| Publisher_xml | – name: 생화학분자생물학회 |
| SSID | ssib044731790 ssj0061272 ssib053376789 |
| Score | 2.430567 |
| Snippet | Histone deacetylases (HDACs) are essential enzymes that play a pivotal role in the epigenetic regulation of gene expression by catalyzing the removal of acetyl... |
| SourceID | kisti kiss |
| SourceType | Open Access Repository Publisher |
| StartPage | 313 |
| SubjectTerms | Fibrosis HDAC Histone deacetylase Non-histone deacetylase Therapeutic target |
| Title | Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases |
| URI | https://kiss.kstudy.com/ExternalLink/Ar?key=4190403 http://click.ndsl.kr/servlet/LinkingDetailView?cn=JAKO202526636037528&dbt=JAKO&org_code=O481&site_code=SS1481&service_code=01 |
| Volume | 58 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVHPJ databaseName: ROAD: Directory of Open Access Scholarly Resources customDbUrl: eissn: 1976-670X dateEnd: 99991231 omitProxy: false ssIdentifier: ssib044731790 issn: 1976-6696 databaseCode: M~E dateStart: 20080101 isFulltext: true titleUrlDefault: https://road.issn.org providerName: ISSN International Centre |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3Nb9MwFLfKQIILghW08TH5gBBoCqSxE9vcQhmqNhg7VKicKseNRbWRTE02LReO_EP8g7yXj8arkIADlyi1nOol76fn9_0IeTYycEbpgHmh1NzjJtKe9pX1_CCV0UJIf1H7IT9_EMfHcjZTJ4PBz64W5vJMZJm8ulLn_5XVsAbMxtLZf2D3-k9hAe6B6XAFtsP1rxiP_aa6KVa1KojNAzIsj9ImLSvQlhtP6-RdPC7QKdBqn6tmKv3GU-hXz_LM637XfR3QR81irLDss9ExXdGC7Z1jB9g27FNcDxm_7SIUfSQqq1Da7B_q9gBFt7SuLrL98dd82Wf3wJZJDoSdOJVFRxU-OcHNX_Lc9V4EYeeOXQtcUIe8KFJtO2xnTfgzV0qH0kGjdEQua2pZ29ObNRXZmwcD2GXYoALeFOyaV0AIpt40BdHXe3BvnI3rjMXD-OgT0g_6DItwbnAgb5CbgQgVitKP3w86Ica5YCOnhyOo0yKqW_o36gFolPVEsfWLN7FzJPD1JnmgJoAVUYDdhMbE0lF8pvfI3dZioXGDtPtkcJpvk2Gc6TL_VtHntM4hroMz2-T2uJsfOCQ_XCDS3NIWQtQFIn1Rw_AlLXMKIKQ9CN0nAITUASHtQPiGuhCkAEHaQZB2EHxApu8PpuOJ10798E7BWPCMTEZsoXjCw0QYkfqB9lOWSME19jI1PLFWYyoXi6RVPuOoQNtIKBUkMpCGPSRbQFG6QyizSplRmKZGSp6YVFrNUwsCyDJj_CTZJUP8vPPzpq_LnINyzH22S_bqzz3PFsXZ_DeMf_SnDY_JnR7rT8hWubpIn5Jb5rJcFqu9Gi6_AP3Qmsc |
| linkProvider | ISSN International Centre |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Contribution+of+histone+deacetylases+%28HDACs%29+to+the+regulation+of+histone+and+non-histone+proteins%3A+implications+for+fibrotic+diseases&rft.jtitle=BMB+reports&rft.au=Sunyoung+Jang&rft.au=Nayun+Choi&rft.au=Jong+Hoon+Park&rft.au=Kyung+Hyun+Yoo&rft.date=2025-08-31&rft.issn=1976-6696&rft.eissn=1976-670X&rft.volume=58&rft.issue=8&rft.spage=313&rft.epage=324&rft_id=info:doi/10.5483%2FBMBRep.2024-0122&rft.externalDBID=n%2Fa&rft.externalDocID=JAKO202526636037528 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1976-6696&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1976-6696&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1976-6696&client=summon |