Publications by authors named "Xinyi Shentu"

Article Synopsis
  • The study explores how liver cells in mammals coordinate their responses during normal function and when faced with challenges, addressing a significant knowledge gap in understanding liver-related diseases.
  • Researchers used advanced techniques, including Stereo-seq and single-cell transcriptomics, to create a detailed atlas of mouse liver homeostasis and regeneration, analyzing a massive dataset of over 473,000 cells.
  • Key findings include identifying the transcriptional cofactor TBL1XR1, which plays a crucial role in linking inflammation to liver cell proliferation, paving the way for future studies on organ physiology and dysfunction.
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Cholestatic liver injuries, characterized by regional damage around the bile ductular region, lack curative therapies and cause considerable mortality. Here we generated a high-definition spatiotemporal atlas of gene expression during cholestatic injury and repair in mice by integrating spatial enhanced resolution omics sequencing and single-cell transcriptomics. Spatiotemporal analyses revealed a key role of cholangiocyte-driven signaling correlating with the periportal damage-repair response.

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Gene loss is common and influences genome evolution trajectories. Multiple adaptive strategies to compensate for gene loss have been observed, including copy number gain of paralogous genes and mutations in genes of the same pathway. By using the Ubl-specific protease 2 (ULP2) eviction model, we identify compensatory mutations in the homologous gene ULP1 by laboratory evolution and find that these mutations are capable of rescuing defects caused by the loss of ULP2.

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Recent studies show branched-chain amino acid (BCAA) catabolic pathway is defective in obese animals and humans, contributing to the pathogenesis of insulin resistance and diabetes. However, in the context of obesity, various processes including the dysfunctional lipid metabolism can affect insulin sensitivity and glycemic regulation. It remains unclear how BCAA catabolic defect may exert direct impacts on glucose metabolism without the disturbance of obesity.

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