YAP and TAZ protect against white adipocyte cell death during obesity

Lei Wang (), ShengPeng Wang (), Yue Shi, Rui Li, Stefan Günther, Yu Ting Ong, Michael Potente, Zuyi Yuan, Enqi Liu and Stefan Offermanns ()
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Lei Wang: Max Planck Institute for Heart and Lung Research
ShengPeng Wang: Max Planck Institute for Heart and Lung Research
Yue Shi: Xi’an Jiaotong University Health Science Center
Rui Li: Max Planck Institute for Heart and Lung Research
Stefan Günther: Max Planck Institute for Heart and Lung Research
Yu Ting Ong: Max Planck Institute for Heart and Lung Research
Michael Potente: Max Planck Institute for Heart and Lung Research
Zuyi Yuan: First Affiliated Hospital of Xi’an Jiaotong University
Enqi Liu: Xi’an Jiaotong University Health Science Center Xi’an Jiaotong University
Stefan Offermanns: Max Planck Institute for Heart and Lung Research

Nature Communications, 2020, vol. 11, issue 1, 1-13

Abstract: Abstract The expansion of the white adipose tissue (WAT) in obesity goes along with increased mechanical, metabolic and inflammatory stress. How adipocytes resist this stress is still poorly understood. Both in human and mouse adipocytes, the transcriptional co-activators YAP/TAZ and YAP/TAZ target genes become activated during obesity. When fed a high-fat diet (HFD), mice lacking YAP/TAZ in white adipocytes develop severe lipodystrophy with adipocyte cell death. The pro-apoptotic factor BIM, which is downregulated in adipocytes of obese mice and humans, is strongly upregulated in YAP/TAZ-deficient adipocytes under HFD, and suppression of BIM expression reduces adipocyte apoptosis. In differentiated adipocytes, TNFα and IL-1β promote YAP/TAZ nuclear translocation via activation of RhoA-mediated actomyosin contractility and increase YAP/TAZ-mediated transcriptional regulation by activation of c-Jun N-terminal kinase (JNK) and AP-1. Our data indicate that the YAP/TAZ signaling pathway may be a target to control adipocyte cell death and compensatory adipogenesis during obesity.

Date: 2020
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DOI: 10.1038/s41467-020-19229-3

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