Senescence induces clonal failure of hepatocyte plasticity and reshapes regenerative lineages.

Qiumin Zheng, Jian Chen, Xinhao Hu, Yulu Zhang, Shijie Yu, Na Sun, Qi-Yue Zhu, Bin Zhao, Xiao Xu, Shengda Lin

Life Sciences Institute, Zhejiang University, Hangzhou, China; Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. · pubmed

Paper

Abstract

Telomere dysregulation is a central driver of cellular senescence and chronic liver disease. Yet how physiological telomeric attrition, rather than uniform telomere loss, leads to hepatic functional decline remains unclear. We therefore investigate how resolvable telomere dysfunction reshapes liver regeneration.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

Physiological telomere shortening induces clonal failure in hepatocyte plasticity, thereby reshaping regenerative lineages and driving liver functional decline. This paper is relevant because it investigates the fundamental mechanism of cellular senescence (telomere attrition) and its direct impact on tissue regeneration, which is a core component of the aging process rather than just a downstream symptom.

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