Smad3 Mediates Diabetic Dyslipidemia and Fatty Liver in db/db Mice by Targeting PPARδ
Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeuti...
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Published in | International journal of molecular sciences Vol. 24; no. 14; p. 11396 |
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Abstract | Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeutic effect on these metabolic abnormalities remains unexplored. These topics were investigated in this study in Smad3 knockout (KO)-
mice and by treating
mice with a Smad3-specific inhibitor SIS3. Compared to Smad3 wild-type (WT)-
mice, Smad3 KO-
mice were protected against dyslipidemia and NAFLD. Similarly, treatment of
mice with SIS3 at week 4 before the onset of type 2 diabetes until week 12 was capable of lowering blood glucose levels and improving diabetic dyslipidemia and NAFLD. In addition, using RNA-sequencing, the potential Smad3-target genes related to lipid metabolism was identified in the liver tissues of Smad3 KO/WT mice, and the regulatory mechanisms were investigated. Mechanistically, we uncovered that Smad3 targeted peroxisome proliferator-activated receptor delta (PPARδ) to induce dyslipidemia and NAFLD in
mice, which was improved by genetically deleting and pharmacologically inhibiting Smad3. |
---|---|
AbstractList | Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeutic effect on these metabolic abnormalities remains unexplored. These topics were investigated in this study in Smad3 knockout (KO)-
db/db
mice and by treating
db/db
mice with a Smad3-specific inhibitor SIS3. Compared to Smad3 wild-type (WT)-
db/db
mice, Smad3 KO-
db/db
mice were protected against dyslipidemia and NAFLD. Similarly, treatment of
db/db
mice with SIS3 at week 4 before the onset of type 2 diabetes until week 12 was capable of lowering blood glucose levels and improving diabetic dyslipidemia and NAFLD. In addition, using RNA-sequencing, the potential Smad3-target genes related to lipid metabolism was identified in the liver tissues of Smad3 KO/WT mice, and the regulatory mechanisms were investigated. Mechanistically, we uncovered that Smad3 targeted peroxisome proliferator-activated receptor delta (PPARδ) to induce dyslipidemia and NAFLD in
db/db
mice, which was improved by genetically deleting and pharmacologically inhibiting Smad3. Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeutic effect on these metabolic abnormalities remains unexplored. These topics were investigated in this study in Smad3 knockout (KO)- mice and by treating mice with a Smad3-specific inhibitor SIS3. Compared to Smad3 wild-type (WT)- mice, Smad3 KO- mice were protected against dyslipidemia and NAFLD. Similarly, treatment of mice with SIS3 at week 4 before the onset of type 2 diabetes until week 12 was capable of lowering blood glucose levels and improving diabetic dyslipidemia and NAFLD. In addition, using RNA-sequencing, the potential Smad3-target genes related to lipid metabolism was identified in the liver tissues of Smad3 KO/WT mice, and the regulatory mechanisms were investigated. Mechanistically, we uncovered that Smad3 targeted peroxisome proliferator-activated receptor delta (PPARδ) to induce dyslipidemia and NAFLD in mice, which was improved by genetically deleting and pharmacologically inhibiting Smad3. Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeutic effect on these metabolic abnormalities remains unexplored. These topics were investigated in this study in Smad3 knockout (KO)-db/db mice and by treating db/db mice with a Smad3-specific inhibitor SIS3. Compared to Smad3 wild-type (WT)-db/db mice, Smad3 KO-db/db mice were protected against dyslipidemia and NAFLD. Similarly, treatment of db/db mice with SIS3 at week 4 before the onset of type 2 diabetes until week 12 was capable of lowering blood glucose levels and improving diabetic dyslipidemia and NAFLD. In addition, using RNA-sequencing, the potential Smad3-target genes related to lipid metabolism was identified in the liver tissues of Smad3 KO/WT mice, and the regulatory mechanisms were investigated. Mechanistically, we uncovered that Smad3 targeted peroxisome proliferator-activated receptor delta (PPARδ) to induce dyslipidemia and NAFLD in db/db mice, which was improved by genetically deleting and pharmacologically inhibiting Smad3. |
Audience | Academic |
Author | Chen, Jiaoyi Lan, Huiyao Chen, Xiaocui Wang, Honglian Huang, Xiaoru He, Huijun Wang, Cheng Xue, Vivian Weiwen Zhong, Yu Tang, Patrick Ming-Kuen |
AuthorAffiliation | 2 Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China; yuzhong@link.cuhk.edu.hk (Y.Z.); honglianwang@swmu.edu.cn (H.W.); chenxiaocui2012@outlook.com (X.C.); margaret.chenjy@link.cuhk.edu.hk (J.C.); xlan@cuhk.edu.hk (X.H.) 4 State Key Laboratory of Translational Oncology, Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong 999077, China; patrick.tang@cuhk.edu.hk (P.M.-K.T.); vivian.xue@connect.polyu.hk (V.W.X.) 1 Division of Nephrology, Department of Medicine, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China; hehuijun@link.cuhk.edu.hk 3 Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China |
AuthorAffiliation_xml | – name: 1 Division of Nephrology, Department of Medicine, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China; hehuijun@link.cuhk.edu.hk – name: 2 Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China; yuzhong@link.cuhk.edu.hk (Y.Z.); honglianwang@swmu.edu.cn (H.W.); chenxiaocui2012@outlook.com (X.C.); margaret.chenjy@link.cuhk.edu.hk (J.C.); xlan@cuhk.edu.hk (X.H.) – name: 4 State Key Laboratory of Translational Oncology, Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong 999077, China; patrick.tang@cuhk.edu.hk (P.M.-K.T.); vivian.xue@connect.polyu.hk (V.W.X.) – name: 3 Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China |
Author_xml | – sequence: 1 givenname: Huijun orcidid: 0000-0003-1910-3897 surname: He fullname: He, Huijun organization: Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China – sequence: 2 givenname: Yu orcidid: 0000-0001-6902-2732 surname: Zhong fullname: Zhong, Yu organization: Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China – sequence: 3 givenname: Honglian surname: Wang fullname: Wang, Honglian organization: Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China – sequence: 4 givenname: Patrick Ming-Kuen orcidid: 0000-0002-3194-3736 surname: Tang fullname: Tang, Patrick Ming-Kuen organization: State Key Laboratory of Translational Oncology, Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong 999077, China – sequence: 5 givenname: Vivian Weiwen orcidid: 0000-0002-0737-3593 surname: Xue fullname: Xue, Vivian Weiwen organization: State Key Laboratory of Translational Oncology, Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong 999077, China – sequence: 6 givenname: Xiaocui surname: Chen fullname: Chen, Xiaocui organization: Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China – sequence: 7 givenname: Jiaoyi orcidid: 0000-0001-5601-9411 surname: Chen fullname: Chen, Jiaoyi organization: Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China – sequence: 8 givenname: Xiaoru surname: Huang fullname: Huang, Xiaoru organization: Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China – sequence: 9 givenname: Cheng orcidid: 0000-0002-1590-7954 surname: Wang fullname: Wang, Cheng organization: Guangdong Provincial Key Laboratory of Biomedical Imaging, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China – sequence: 10 givenname: Huiyao orcidid: 0000-0003-4283-9755 surname: Lan fullname: Lan, Huiyao organization: Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong 999077, China |
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Keywords | Smad3 inhibitor treatment Smad3 fatty liver dyslipidemia diabetes |
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Snippet | Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3... |
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SubjectTerms | Blood sugar Cholesterol Diabetes Diabetic nephropathy Diagnostic reagents industry Disease dyslipidemia Fatty acids Fatty liver Health aspects High density lipoprotein Hyperglycemia Insulin resistance Lipids Liver Metabolic disorders Physiological aspects Scientific equipment and supplies industry Smad3 Smad3 inhibitor Transforming growth factors treatment Type 2 diabetes |
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Title | Smad3 Mediates Diabetic Dyslipidemia and Fatty Liver in db/db Mice by Targeting PPARδ |
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