New Insights into the Role of KLF10 in Tissue Fibrosis
Fibrosis, characterized by excessive extracellular matrix accumulation, disrupts normal tissue architecture, causes organ dysfunction, and contributes to numerous chronic diseases. This review focuses on Krüppel-like factor 10 (KLF10), a transcription factor significantly induced by transforming gro...
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| Format: | Article |
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MDPI AG
2024-01-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/25/2/1276 |
| _version_ | 1797339739431370752 |
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| author | Uzma Yaseen Soonjae Hwang Sangbin Park Soo-Bin Kim Ho-Jae Lee Ji-Young Cha |
| author_facet | Uzma Yaseen Soonjae Hwang Sangbin Park Soo-Bin Kim Ho-Jae Lee Ji-Young Cha |
| author_sort | Uzma Yaseen |
| collection | DOAJ |
| description | Fibrosis, characterized by excessive extracellular matrix accumulation, disrupts normal tissue architecture, causes organ dysfunction, and contributes to numerous chronic diseases. This review focuses on Krüppel-like factor 10 (KLF10), a transcription factor significantly induced by transforming growth factor-β (TGF-β), and its role in fibrosis pathogenesis and progression across various tissues. KLF10, initially identified as TGF-β-inducible early gene-1 (TIEG1), is involved in key biological processes including cell proliferation, differentiation, apoptosis, and immune responses. Our analysis investigated KLF10 gene and protein structures, interaction partners, and context-dependent functions in fibrotic diseases. This review highlights recent findings that underscore KLF10 interaction with pivotal signaling pathways, such as TGF-β, and the modulation of gene expression in fibrotic tissues. We examined the dual role of KLF10 in promoting and inhibiting fibrosis depending on tissue type and fibrotic context. This review also discusses the therapeutic potential of targeting KLF10 in fibrotic diseases, based on its regulatory role in key pathogenic mechanisms. By consolidating current research, this review aims to enhance the understanding of the multifaceted role of KLF10 in fibrosis and stimulate further research into its potential as a therapeutic target in combating fibrotic diseases. |
| first_indexed | 2024-03-08T09:52:43Z |
| format | Article |
| id | doaj.art-46ca4557c6c045929630534038e92a5f |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-08T09:52:43Z |
| publishDate | 2024-01-01 |
| publisher | MDPI AG |
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| series | International Journal of Molecular Sciences |
| spelling | doaj.art-46ca4557c6c045929630534038e92a5f2024-01-29T13:59:12ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672024-01-01252127610.3390/ijms25021276New Insights into the Role of KLF10 in Tissue FibrosisUzma Yaseen0Soonjae Hwang1Sangbin Park2Soo-Bin Kim3Ho-Jae Lee4Ji-Young Cha5Department of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Republic of KoreaDepartment of Biochemistry, Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, Incheon 21999, Republic of KoreaDepartment of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Republic of KoreaDepartment of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Republic of KoreaDepartment of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Republic of KoreaDepartment of Health Sciences and Technology, GAIHST, Gachon University, Incheon 21999, Republic of KoreaFibrosis, characterized by excessive extracellular matrix accumulation, disrupts normal tissue architecture, causes organ dysfunction, and contributes to numerous chronic diseases. This review focuses on Krüppel-like factor 10 (KLF10), a transcription factor significantly induced by transforming growth factor-β (TGF-β), and its role in fibrosis pathogenesis and progression across various tissues. KLF10, initially identified as TGF-β-inducible early gene-1 (TIEG1), is involved in key biological processes including cell proliferation, differentiation, apoptosis, and immune responses. Our analysis investigated KLF10 gene and protein structures, interaction partners, and context-dependent functions in fibrotic diseases. This review highlights recent findings that underscore KLF10 interaction with pivotal signaling pathways, such as TGF-β, and the modulation of gene expression in fibrotic tissues. We examined the dual role of KLF10 in promoting and inhibiting fibrosis depending on tissue type and fibrotic context. This review also discusses the therapeutic potential of targeting KLF10 in fibrotic diseases, based on its regulatory role in key pathogenic mechanisms. By consolidating current research, this review aims to enhance the understanding of the multifaceted role of KLF10 in fibrosis and stimulate further research into its potential as a therapeutic target in combating fibrotic diseases.https://www.mdpi.com/1422-0067/25/2/1276fibrosisKrüppel-like factor 10TGF-βNAFLDNASH |
| spellingShingle | Uzma Yaseen Soonjae Hwang Sangbin Park Soo-Bin Kim Ho-Jae Lee Ji-Young Cha New Insights into the Role of KLF10 in Tissue Fibrosis International Journal of Molecular Sciences fibrosis Krüppel-like factor 10 TGF-β NAFLD NASH |
| title | New Insights into the Role of KLF10 in Tissue Fibrosis |
| title_full | New Insights into the Role of KLF10 in Tissue Fibrosis |
| title_fullStr | New Insights into the Role of KLF10 in Tissue Fibrosis |
| title_full_unstemmed | New Insights into the Role of KLF10 in Tissue Fibrosis |
| title_short | New Insights into the Role of KLF10 in Tissue Fibrosis |
| title_sort | new insights into the role of klf10 in tissue fibrosis |
| topic | fibrosis Krüppel-like factor 10 TGF-β NAFLD NASH |
| url | https://www.mdpi.com/1422-0067/25/2/1276 |
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