A brain-to-liver signal mediates the inhibition of liver regeneration under chronic stress in mice

Yanyu Zhou, Xiaoqi Lin, Yingfu Jiao, Dan Yang, Zhengyu Li, Ling Zhu, Yixuan Li, Suqing Yin, Quanfu Li, Saihong Xu, Dan Tang, Song Zhang, Weifeng Yu (), Po Gao () and Liqun Yang ()
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Yanyu Zhou: Shanghai Jiao Tong University School of Medicine
Xiaoqi Lin: Shanghai Jiao Tong University School of Medicine
Yingfu Jiao: Shanghai Jiao Tong University School of Medicine
Dan Yang: Shanghai Jiao Tong University School of Medicine
Zhengyu Li: Shanghai Jiao Tong University School of Medicine
Ling Zhu: Shanghai Jiao Tong University School of Medicine
Yixuan Li: Shanghai Jiao Tong University School of Medicine
Suqing Yin: Shanghai Jiao Tong University School of Medicine
Quanfu Li: Shanghai Jiao Tong University School of Medicine
Saihong Xu: Shanghai Jiao Tong University School of Medicine
Dan Tang: Shanghai Jiao Tong University School of Medicine
Song Zhang: Shanghai Jiao Tong University School of Medicine
Weifeng Yu: Shanghai Jiao Tong University School of Medicine
Po Gao: Shanghai Jiao Tong University School of Medicine
Liqun Yang: Shanghai Jiao Tong University School of Medicine

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract As the ability of liver regeneration is pivotal for liver disease patients, it will be of high significance and importance to identify the missing piece of the jigsaw influencing the liver regeneration. Here, we report that chronic stress impairs the liver regeneration capacity after partial hepatectomy with increased mortality in male mice. Anatomical tracing and functional mapping identified a neural circuit from noradrenergic neurons in the locus coeruleus (LC) to serotonergic neurons in the rostral medullary raphe region (rMR), which critically contributes to the inhibition of liver regeneration under chronic stress. In addition, hepatic sympathetic nerves were shown to be critical for the inhibitory effects on liver regeneration by releasing norepinephrine (NE), which acts on adrenergic receptor β2 (ADRB2) to block the proinflammatory macrophage activation. Collectively, we reveal a “brain-to-liver” neural connection that mediates chronic stress-evoked deficits in liver regeneration, thus shedding important insights into hepatic disease therapy.

Date: 2024
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DOI: 10.1038/s41467-024-54827-5

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