Experimental and Molecular Medicine (Jan 2020)

TGF-β1/IL-11/MEK/ERK signaling mediates senescence-associated pulmonary fibrosis in a stress-induced premature senescence model of Bmi-1 deficiency

  • Haiyun Chen,
  • Hongjie Chen,
  • Jialong Liang,
  • Xin Gu,
  • Jiawen Zhou,
  • Chunfeng Xie,
  • Xianhui Lv,
  • Rong Wang,
  • Qing Li,
  • Zhiyuan Mao,
  • Haijian Sun,
  • Guoping Zuo,
  • Dengshun Miao,
  • Jianliang Jin

DOI
https://doi.org/10.1038/s12276-019-0371-7
Journal volume & issue
Vol. 52, no. 1
pp. 130 – 151

Abstract

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Lung fibrosis: calling TIME on disease progression Targeting cellular signals that are increased in lung fibrosis may help halt disease progression. The build-up of scarred and thickened tissues in the lungs associated with aging and cellular deterioration is known as senescence-associated pulmonary fibrosis (SAPF). There are limited treatment options, and Jianliang Jin at Nanjing Medical University, China, and co-workers believe that targeting a complex of cellular signaling pathways called TGF-β1/IL-11/MEK/ERK (TIME) signals, the disruption of which affects tissue homeostasis, may hold the key to tackling the disease. The team conducted experiments on mouse models of SAPF, deficient in a gene called Bmi-1. The protein encoded by Bmi-1 is critical for cell division and DNA damage repair. In the Bmi-1-deficient mice, the researchers found that TIME signals were overexpressed, resulting in premature cellular deterioration, increased inflammation and accelerated collagen production.