# Red Blood Cells in Normal and Pathological States: Redox Reactions of Hemoglobin

**Authors:** Krzysztof Gwozdzinski, Anna Pieniazek, Lukasz Gwozdzinski

PMC · DOI: 10.3390/molecules31030444 · Molecules · 2026-01-27

## TL;DR

This review discusses how red blood cells change in health and disease, focusing on their role in diabetes and how oxidative damage affects oxygen transport.

## Contribution

The paper provides a comprehensive overview of RBC alterations in type 2 diabetes and their redox-related consequences.

## Key findings

- RBC deformability changes due to membrane and cytoskeleton damage affect microcirculation.
- Oxidative changes in hemoglobin impair oxygen transport, leading to ischemia and hypoxia.
- Hemoglobin and heme contribute to oxidative damage in RBCs and other biological materials.

## Abstract

Red blood cells (RBCs) play a key role in vascular origin pathologies such as nephropathy, retinopathy, and neuropathy. Altered RBCs also occur in the case of hereditary spherocytosis, hemoglobinopathies, sickle cell disease, thalassemia and hemolytic anemia. The consequence of damage to the cell membrane and cytoskeleton are changes in RBC deformability, which play an important role in microcirculation. In turn, oxidative changes in hemoglobin lead to impaired oxygen transport to cells and tissues and, consequently, to ischemia and hypoxia. In this review, we discuss the structure of normal and pathological RBCs, including, more broadly, red blood cells occurring in type 2 diabetes. We present factors that play a major role in RBC damage in this pathology. Finally, we characterize the participation of hemoglobin and heme in the induction of oxidative damage to biological material, including RBCs.

## Linked entities

- **Proteins:** HB1 (hemoglobin 1)
- **Chemicals:** heme (PubChem CID 4973)
- **Diseases:** retinopathy (MONDO:0005283), neuropathy (MONDO:0005244), hereditary spherocytosis (MONDO:0019350), sickle cell disease (MONDO:0011382), thalassemia (MONDO:0000984), hemolytic anemia (MONDO:0003664), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Diseases:** sickle cell disease (MESH:D000755), nephropathy (MESH:D007674), thalassemia (MESH:D013789), hereditary spherocytosis (MESH:D013103), hypoxia (MESH:D000860), ischemia (MESH:D007511), neuropathy (MESH:D009422), type 2 diabetes (MESH:D003924), hemoglobinopathies (MESH:D006453), retinopathy (MESH:D058437), hemolytic anemia (MESH:D000743)
- **Chemicals:** heme (MESH:D006418), oxygen (MESH:D010100)

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12899599/full.md

## References

114 references — full list in the complete paper: https://tomesphere.com/paper/PMC12899599/full.md

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Source: https://tomesphere.com/paper/PMC12899599