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May 9, 20260 citationsOpen Access

Functional Inversion of Tumor-Associated Macrophages into Iron-Releasing Oxidative Amplifiers: The CD163–HO-1 Bottleneck Hypothesis as a Mechanistic Core of the Sugar–Iron Bomb Model

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MYMohammed Fuad Yousef

Key Points

  • This project investigates how tumor-associated macrophages can switch roles under iron stress, contributing to disease mechanisms.
  • Theoretical model development based on the CD163–HO-1 bottleneck hypothesis.
  • Linking macrophage phenotype to iron dysregulation and genomic instability.
  • Implementation of predictions within the tumor microenvironment framework.
  • Proposed functional inversion of macrophages leads to iron dysregulation and enhanced oxidative stress in tumors.
  • Multiple testable predictions generated to support the CD163–HO-1 hypothesis.
  • Evidence indicating that this mechanism influences tumor genomic stability.

Abstract

This project proposes the CD163–HO-1 bottleneck hypothesis as a molecular mechanism underlying pathological iron dysregulation within the Sugar–Iron Bomb framework. Under sustained hemolytic stress, tumor-associated macrophages may transition from protective hemoglobin scavengers into pathological oxidative amplifiers, a process termed "functional inversion." The model generates multiple testable predictions linking macrophage phenotype, iron dysregulation, and genomic instability within the tumor microenvironment. **Related Publication (Zenodo):** - Primary: https://doi.org/10.5281/zenodo.20068648

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Cite This Study

Mohammed Fuad Yousef (2026) studied this question.

synapsesocial.com/papers/69fed10fb9154b0b828784bdhttps://doi.org/10.17605/osf.io/xvn8c
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