The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7
© 2024. The Author(s)..
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:23 |
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| Enthalten in: |
Cardiovascular diabetology - 23(2024), 1 vom: 09. Jan., Seite 21 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Chen, Wujun [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 11.01.2024 Date Revised 13.03.2024 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1186/s12933-024-02119-z |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
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| 100 | 1 | |a Chen, Wujun |e verfasserin |4 aut | |
| 245 | 1 | 4 | |a The translational potential of miR-26 in atherosclerosis and development of agents for its target genes ACC1/2, COL1A1, CPT1A, FBP1, DGAT2, and SMAD7 |
| 264 | 1 | |c 2024 | |
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| 500 | |a Date Completed 11.01.2024 | ||
| 500 | |a Date Revised 13.03.2024 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2024. The Author(s). | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a COL1A1 | |
| 650 | 4 | |a DGAT2 | |
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| 650 | 7 | |a Diacylglycerol O-Acyltransferase |2 NLM | |
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| 650 | 7 | |a MicroRNAs |2 NLM | |
| 650 | 7 | |a MK-0616 |2 NLM | |
| 650 | 7 | |a PCSK9 protein, human |2 NLM | |
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| 650 | 7 | |a Proprotein Convertase 9 |2 NLM | |
| 650 | 7 | |a EC 3.4.21.- |2 NLM | |
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| 650 | 7 | |a SMAD7 protein, human |2 NLM | |
| 650 | 7 | |a MIRN26 microRNA, human |2 NLM | |
| 700 | 1 | |a Wu, Xiaolin |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Jianxia |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Xiaolei |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Zhu |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Jianfeng |e verfasserin |4 aut | |
| 700 | 1 | |a Shao, Yingchun |e verfasserin |4 aut | |
| 700 | 1 | |a Hao, Minglu |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Shuangshuang |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Weichao |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Yanhong |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Miao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhu, Meng |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Chao |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Yudong |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jie |e verfasserin |4 aut | |
| 700 | 1 | |a Xing, Dongming |e verfasserin |4 aut | |
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