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Related Experiment Video

Updated: Jul 6, 2026

Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes
08:45

Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes

Published on: May 10, 2022

Non-transferrin-bound iron uptake by cardiomyocytes.

Qian Guo1,2, Yao-Zhao Li3,4, Zhong-Ming Qian5,6

  • 1Mental Health Center, Shanghai University School of Medicine, Shanghai, China. qian_guo@shu.edu.cn.

Journal of Molecular Medicine (Berlin, Germany)
|July 4, 2026
PubMed
Summary

Iron overload causes heart disease by allowing non-transferrin-bound iron (NTBI) into cardiomyocytes. This review synthesizes current knowledge on NTBI uptake pathways, aiding future research in iron-overload cardiomyopathy.

Keywords:
CardiomyocytesDivalent metal transporter 1 (DMT1)Iron overload cardiomyopathyL-type Ca2 + channels (LTCC)Lipocalin-2 (LCN-2) / lipocalin 2 receptor (LCN-2R) systemNon-transferrin-bound iron (NTBI)T-type Ca2 + channels (TTCC)ZIP14 (SLC39A14)

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Related Experiment Videos

Last Updated: Jul 6, 2026

Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes
08:45

Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes

Published on: May 10, 2022

Measurement of Tissue Non-Heme Iron Content using a Bathophenanthroline-Based Colorimetric Assay
05:08

Measurement of Tissue Non-Heme Iron Content using a Bathophenanthroline-Based Colorimetric Assay

Published on: January 31, 2022

Area of Science:

  • Cardiology
  • Biochemistry
  • Cell Biology

Background:

  • Iron overload leads to non-transferrin-bound iron (NTBI) accumulation in cardiomyocytes.
  • NTBI contributes to reactive oxygen species generation and iron-overload cardiomyopathy.
  • Understanding NTBI uptake mechanisms is crucial for managing heart disease.

Purpose of the Study:

  • To systematically summarize current research on cardiomyocyte NTBI uptake pathways.
  • To identify key molecular transporters involved in cardiac iron entry.
  • To highlight knowledge gaps and suggest future research directions.

Main Methods:

  • Literature review and synthesis of existing studies.
  • Focus on identified NTBI transport routes in cardiomyocytes.
  • Analysis of molecular mechanisms and their role in iron homeostasis.

Main Results:

  • Multiple pathways mediate NTBI uptake, including L-type Ca2+ channels (LTCC), T-type Ca2+ channels (TTCC), divalent metal transporter 1 (DMT1), the Lipocalin-2/Lipocalin-2 receptor (LCN-2/LCN-2R) system, and ZIP14 (SLC39A14).
  • These transporters play distinct roles in cellular iron acquisition under overload conditions.
  • The precise contribution and regulation of each pathway require further investigation.

Conclusions:

  • Cardiomyocytes utilize several distinct transporters for NTBI uptake.
  • Further research is needed to fully elucidate the roles of LTCC, TTCC, DMT1, LCN-2/LCN-2R, and ZIP14 in iron-overload cardiomyopathy.
  • Addressing these knowledge gaps is essential for developing targeted therapies.