Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation
Inflammation contributes to the development of metabolic disease through incompletely understood mechanisms. Here the authors report that deletion of the transcription factor KLF2 in myeloid cells leads to increased feeding and weight gain in mice with concomitant peripheral and central tissue infla...
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Nature Publishing Group
2020-11-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-020-19760-3 |
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doaj-47134c5fedda43b5b639f09776f89f282021-05-11T08:42:30ZengNature Publishing GroupNature Communications2041-17232020-11-0111111110.1038/s41467-020-19760-3Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammationDavid R. Sweet0Neelakantan T. Vasudevan1Liyan Fan2Chloe E. Booth3Komal S. Keerthy4Xudong Liao5Vinesh Vinayachandran6Yoichi Takami7Derin Tugal8Nikunj Sharma9E. Ricky Chan10Lilei Zhang11Yulan Qing12Stanton L. Gerson13Chen Fu14Anthony Wynshaw-Boris15Panjamaporn Sangwung16Lalitha Nayak17Paul Holvoet18Keiichiro Matoba19Yuan Lu20Guangjin Zhou21Mukesh K. Jain22Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterDepartment of Geriatric Medicine, Osaka University Graduate School of MedicineDepartment of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical SchoolDBPAP/OVRR/CBER, Food and Drug AdministrationInstitute for Computational Biology, Case Western Reserve UniversityDepartment of Molecular and Human Genetics, Baylor College of MedicineCase Comprehensive Cancer Center, Case Western Reserve UniversityCase Comprehensive Cancer Center, Case Western Reserve UniversityDepartment of Genetics and Genome Sciences, Case Western Reserve University, and University Hospitals Cleveland Medical CenterDepartment of Genetics and Genome Sciences, Case Western Reserve University, and University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterDivision of Hematology and Oncology, University Hospitals Cleveland Medical CenterExperimental Cardiology, Department of Cardiovascular Sciences, KU LeuvenCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterCase Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical CenterInflammation contributes to the development of metabolic disease through incompletely understood mechanisms. Here the authors report that deletion of the transcription factor KLF2 in myeloid cells leads to increased feeding and weight gain in mice with concomitant peripheral and central tissue inflammation, while overexpression protects against diet-induced metabolic disease.https://doi.org/10.1038/s41467-020-19760-3 |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
David R. Sweet Neelakantan T. Vasudevan Liyan Fan Chloe E. Booth Komal S. Keerthy Xudong Liao Vinesh Vinayachandran Yoichi Takami Derin Tugal Nikunj Sharma E. Ricky Chan Lilei Zhang Yulan Qing Stanton L. Gerson Chen Fu Anthony Wynshaw-Boris Panjamaporn Sangwung Lalitha Nayak Paul Holvoet Keiichiro Matoba Yuan Lu Guangjin Zhou Mukesh K. Jain |
| spellingShingle |
David R. Sweet Neelakantan T. Vasudevan Liyan Fan Chloe E. Booth Komal S. Keerthy Xudong Liao Vinesh Vinayachandran Yoichi Takami Derin Tugal Nikunj Sharma E. Ricky Chan Lilei Zhang Yulan Qing Stanton L. Gerson Chen Fu Anthony Wynshaw-Boris Panjamaporn Sangwung Lalitha Nayak Paul Holvoet Keiichiro Matoba Yuan Lu Guangjin Zhou Mukesh K. Jain Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation Nature Communications |
| author_facet |
David R. Sweet Neelakantan T. Vasudevan Liyan Fan Chloe E. Booth Komal S. Keerthy Xudong Liao Vinesh Vinayachandran Yoichi Takami Derin Tugal Nikunj Sharma E. Ricky Chan Lilei Zhang Yulan Qing Stanton L. Gerson Chen Fu Anthony Wynshaw-Boris Panjamaporn Sangwung Lalitha Nayak Paul Holvoet Keiichiro Matoba Yuan Lu Guangjin Zhou Mukesh K. Jain |
| author_sort |
David R. Sweet |
| title |
Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation |
| title_short |
Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation |
| title_full |
Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation |
| title_fullStr |
Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation |
| title_full_unstemmed |
Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation |
| title_sort |
myeloid krüppel-like factor 2 is a critical regulator of metabolic inflammation |
| publisher |
Nature Publishing Group |
| series |
Nature Communications |
| issn |
2041-1723 |
| publishDate |
2020-11-01 |
| description |
Inflammation contributes to the development of metabolic disease through incompletely understood mechanisms. Here the authors report that deletion of the transcription factor KLF2 in myeloid cells leads to increased feeding and weight gain in mice with concomitant peripheral and central tissue inflammation, while overexpression protects against diet-induced metabolic disease. |
| url |
https://doi.org/10.1038/s41467-020-19760-3 |
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