Commentary 10.1172/JCI124583
1Guangzhou Institutes of Biomedicine and Health,
2CAS Key Laboratory of Regenerative Biology, Guangzhou, China.
3Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine,
4Guangzhou Regenerative Medicine and Health, Guangdong Laboratory, Guangzhou, China.
Address correspondence to: Duanqing Pei, Guangzhou Institutes of Biomedicine and Health, CAS, No. 190, KaiYuan Road, Science Park, Guangzhou, Guangdong 510530, China. Phone: 86.20.32015231; Email: pei_duanqing@gibh.ac.cn.
Find articles by Wang, T. in: JCI | PubMed | Google Scholar
1Guangzhou Institutes of Biomedicine and Health,
2CAS Key Laboratory of Regenerative Biology, Guangzhou, China.
3Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine,
4Guangzhou Regenerative Medicine and Health, Guangdong Laboratory, Guangzhou, China.
Address correspondence to: Duanqing Pei, Guangzhou Institutes of Biomedicine and Health, CAS, No. 190, KaiYuan Road, Science Park, Guangzhou, Guangdong 510530, China. Phone: 86.20.32015231; Email: pei_duanqing@gibh.ac.cn.
Find articles by Pei, D. in: JCI | PubMed | Google Scholar
First published November 26, 2018 - More info
Insulin-secreting β cell loss or dysfunction is a feature of both type 1 and type 2 diabetes. Strategies to restore β cell mass are limited, as sources of healthy islets are scarce and mature β cells are not readily expanded in vitro. In this issue of the JCI, Ou et al. report that mature β cell expansion can be induced in situ through epigenetic editing of regulatory elements in pancreatic tissue. Specifically, hypomethylation at imprinting control region 2 (ICR2) in human islets promoted β cell expansion. Importantly, transplantation of these epigenetically edited islets into diabetic mice reduced blood glucose levels. Together, these results support further evaluation of this strategy for restoring β cell mass in patients with diabetes.
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