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August 2, 2026Cell ReportsOpen Access

SLC39A11 mediates intracellular manganese partitioning and adaptive iron transport

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Authors

YCYanmei CuiFDFan DuJWJuan Wang

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Overview

Randomized trial demonstrates that SLC39A11 influences metal transport in mice, suggesting new therapeutic targets for fibrosis.

Key Points

  • This research investigates the role of SLC39A11 in manganese partitioning and iron transport within cells, particularly its impact on fibrosis.
  • Characterized SLC39A11 functions as a metal transporter in vitro and in vivo.
  • Observed effects of AAV8-mediated ZIP11 expression on liver fibrosis induced by CCl4 in mice.
  • Examined the interaction between ZIP11 and manganese transporter TMEM165 regarding manganese sensitivity.
  • AAV8-mediated ZIP11 expression significantly suppresses liver fibrosis in CCl4-treated mice (p<0.01).
  • ZIP11 deficiency reduces ER/Golgi Mn2+ levels and increases cytosolic Mn2+, enhancing toxicity.
  • ZIP11 and TMEM165 double deficiency exacerbates manganese sensitivity, indicating functional synergy.

Cite This Study

Cui et al. (2026) studied this question.

synapsesocial.com/papers/6a6eea5d1b0468a7eeab2bb4https://doi.org/10.1016/j.celrep.2026.117781
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Also Consider

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