Nature Communications (Nov 2020)
Myeloid Krüppel-like factor 2 is a critical regulator of metabolic inflammation
- 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
Affiliations
- David R. Sweet
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Neelakantan T. Vasudevan
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Liyan Fan
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Chloe E. Booth
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Komal S. Keerthy
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Xudong Liao
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Vinesh Vinayachandran
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Yoichi Takami
- Department of Geriatric Medicine, Osaka University Graduate School of Medicine
- Derin Tugal
- Department of Medicine, Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School
- Nikunj Sharma
- DBPAP/OVRR/CBER, Food and Drug Administration
- E. Ricky Chan
- Institute for Computational Biology, Case Western Reserve University
- Lilei Zhang
- Department of Molecular and Human Genetics, Baylor College of Medicine
- Yulan Qing
- Case Comprehensive Cancer Center, Case Western Reserve University
- Stanton L. Gerson
- Case Comprehensive Cancer Center, Case Western Reserve University
- Chen Fu
- Department of Genetics and Genome Sciences, Case Western Reserve University, and University Hospitals Cleveland Medical Center
- Anthony Wynshaw-Boris
- Department of Genetics and Genome Sciences, Case Western Reserve University, and University Hospitals Cleveland Medical Center
- Panjamaporn Sangwung
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Lalitha Nayak
- Division of Hematology and Oncology, University Hospitals Cleveland Medical Center
- Paul Holvoet
- Experimental Cardiology, Department of Cardiovascular Sciences, KU Leuven
- Keiichiro Matoba
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Yuan Lu
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Guangjin Zhou
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- Mukesh K. Jain
- Case Cardiovascular Research Institute, Case Western Reserve University, and Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center
- DOI
- https://doi.org/10.1038/s41467-020-19760-3
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 11
Abstract
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.
