The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7
Abstract Atherosclerosis is one of the leading causes of death worldwide. miR-26 is a potential biomarker of atherosclerosis. Standardized diagnostic tests for miR-26 (MIR26-DX) have been developed, but the fastest progress has been in predicting the efficacy of IFN-α therapy for hepatocellular carc...
| Main Authors: | , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2024-01-01
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| Series: | Cardiovascular Diabetology |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12933-024-02119-z |
| _version_ | 1827382410764877824 |
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| author | Wujun Chen Xiaolin Wu Jianxia Hu Xiaolei Liu Zhu Guo Jianfeng Wu Yingchun Shao Minglu Hao Shuangshuang Zhang Weichao Hu Yanhong Wang Miao Zhang Meng Zhu Chao Wang Yudong Wu Jie Wang Dongming Xing |
| author_facet | Wujun Chen Xiaolin Wu Jianxia Hu Xiaolei Liu Zhu Guo Jianfeng Wu Yingchun Shao Minglu Hao Shuangshuang Zhang Weichao Hu Yanhong Wang Miao Zhang Meng Zhu Chao Wang Yudong Wu Jie Wang Dongming Xing |
| author_sort | Wujun Chen |
| collection | DOAJ |
| description | Abstract Atherosclerosis is one of the leading causes of death worldwide. miR-26 is a potential biomarker of atherosclerosis. Standardized diagnostic tests for miR-26 (MIR26-DX) have been developed, but the fastest progress has been in predicting the efficacy of IFN-α therapy for hepatocellular carcinoma (HCC, phase 3). MiR-26 slows atherosclerosis development by suppressing ACC1/2, ACLY, ACSL3/4, ALDH3A2, ALPL, BMP2, CD36, COL1A1, CPT1A, CTGF, DGAT2, EHHADH, FAS, FBP1, GATA4, GSK3β, G6PC, Gys2, HMGA1, HMGB1, LDLR, LIPC, IL-1β, IL-6, JAG2, KCNJ2, MALT1, β-MHC, NF-κB, PCK1, PLCβ1, PYGL, RUNX2, SCD1, SMAD1/4/5/7, SREBF1, TAB3, TAK1, TCF7L2, and TNF-α expression. Many agents targeting these genes, such as the ACC1/2 inhibitors GS-0976, PF-05221304, and MK-4074; the DGAT2 inhibitors IONIS-DGAT2Rx, PF-06427878, PF-0685571, and PF-07202954; the COL1A1 inhibitor HT-100; the stimulants 68Ga-CBP8 and RCT-01; the CPT1A inhibitors etomoxir, perhexiline, and teglicar; the FBP1 inhibitors CS-917 and MB07803; and the SMAD7 inhibitor mongersen, have been investigated in clinical trials. Interestingly, miR-26 better reduced intima-media thickness (IMT) than PCSK9 or CT-1 knockout. Many PCSK9 inhibitors, including alirocumab, evolocumab, inclisiran, AZD8233, Civi-007, MK-0616, and LIB003, have been investigated in clinical trials. Recombinant CT-1 was also investigated in clinical trials. Therefore, miR-26 is a promising target for agent development. miR-26 promotes foam cell formation by reducing ABCA1 and ARL4C expression. Multiple materials can be used to deliver miR-26, but it is unclear which material is most suitable for mass production and clinical applications. This review focuses on the potential use of miR-26 in treating atherosclerosis to support the development of agents targeting it. |
| first_indexed | 2024-03-08T14:19:13Z |
| format | Article |
| id | doaj.art-7b161dbc163f4e7a9a4ed16ae9ac1163 |
| institution | Directory Open Access Journal |
| issn | 1475-2840 |
| language | English |
| last_indexed | 2024-03-08T14:19:13Z |
| publishDate | 2024-01-01 |
| publisher | BMC |
| record_format | Article |
| series | Cardiovascular Diabetology |
| spelling | doaj.art-7b161dbc163f4e7a9a4ed16ae9ac11632024-01-14T12:10:52ZengBMCCardiovascular Diabetology1475-28402024-01-0123112110.1186/s12933-024-02119-zThe translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7Wujun Chen0Xiaolin Wu1Jianxia Hu2Xiaolei Liu3Zhu Guo4Jianfeng Wu5Yingchun Shao6Minglu Hao7Shuangshuang Zhang8Weichao Hu9Yanhong Wang10Miao Zhang11Meng Zhu12Chao Wang13Yudong Wu14Jie Wang15Dongming Xing16Cancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteDepartment of Endocrinology, The Affiliated Hospital of Qingdao UniversityDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Qingdao UniversityCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteDepartment of Cardiology, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Key Laboratory of Heart Failure Prevention & Treatment of Hengyang, Clinical Medicine Research Center of Arteriosclerotic Disease of Hunan ProvinceCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteCancer Institute, Department of Orthopaedics, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao Cancer InstituteAbstract Atherosclerosis is one of the leading causes of death worldwide. miR-26 is a potential biomarker of atherosclerosis. Standardized diagnostic tests for miR-26 (MIR26-DX) have been developed, but the fastest progress has been in predicting the efficacy of IFN-α therapy for hepatocellular carcinoma (HCC, phase 3). MiR-26 slows atherosclerosis development by suppressing ACC1/2, ACLY, ACSL3/4, ALDH3A2, ALPL, BMP2, CD36, COL1A1, CPT1A, CTGF, DGAT2, EHHADH, FAS, FBP1, GATA4, GSK3β, G6PC, Gys2, HMGA1, HMGB1, LDLR, LIPC, IL-1β, IL-6, JAG2, KCNJ2, MALT1, β-MHC, NF-κB, PCK1, PLCβ1, PYGL, RUNX2, SCD1, SMAD1/4/5/7, SREBF1, TAB3, TAK1, TCF7L2, and TNF-α expression. Many agents targeting these genes, such as the ACC1/2 inhibitors GS-0976, PF-05221304, and MK-4074; the DGAT2 inhibitors IONIS-DGAT2Rx, PF-06427878, PF-0685571, and PF-07202954; the COL1A1 inhibitor HT-100; the stimulants 68Ga-CBP8 and RCT-01; the CPT1A inhibitors etomoxir, perhexiline, and teglicar; the FBP1 inhibitors CS-917 and MB07803; and the SMAD7 inhibitor mongersen, have been investigated in clinical trials. Interestingly, miR-26 better reduced intima-media thickness (IMT) than PCSK9 or CT-1 knockout. Many PCSK9 inhibitors, including alirocumab, evolocumab, inclisiran, AZD8233, Civi-007, MK-0616, and LIB003, have been investigated in clinical trials. Recombinant CT-1 was also investigated in clinical trials. Therefore, miR-26 is a promising target for agent development. miR-26 promotes foam cell formation by reducing ABCA1 and ARL4C expression. Multiple materials can be used to deliver miR-26, but it is unclear which material is most suitable for mass production and clinical applications. This review focuses on the potential use of miR-26 in treating atherosclerosis to support the development of agents targeting it.https://doi.org/10.1186/s12933-024-02119-zmiR-26IFN-α therapyCOL1A1FBP1DGAT2SMAD7 |
| spellingShingle | Wujun Chen Xiaolin Wu Jianxia Hu Xiaolei Liu Zhu Guo Jianfeng Wu Yingchun Shao Minglu Hao Shuangshuang Zhang Weichao Hu Yanhong Wang Miao Zhang Meng Zhu Chao Wang Yudong Wu Jie Wang Dongming Xing The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7 Cardiovascular Diabetology miR-26 IFN-α therapy COL1A1 FBP1 DGAT2 SMAD7 |
| title | The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7 |
| title_full | The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7 |
| title_fullStr | The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7 |
| title_full_unstemmed | The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7 |
| title_short | The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7 |
| title_sort | translational potential of mir 26 in atherosclerosis and development of agents for its target genes acc1 2 col1a1 cpt1a fbp1 dgat2 and smad7 |
| topic | miR-26 IFN-α therapy COL1A1 FBP1 DGAT2 SMAD7 |
| url | https://doi.org/10.1186/s12933-024-02119-z |
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