Biomechanics of Red Blood Cells, Neutrophils, and Macrophages Under Oxidative Stress and Inflammation: A Narrative Review.
- 1Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.
- 2Department of Medical and Biological Physics, Sechenov First Moscow State Medical University, 119991 Moscow, Russia.
Abstract
This narrative review summarizes current findings on the biomechanics of red blood cells (RBCs), neutrophils, and macrophages under oxidative stress and inflammation. Its cross-cell framework considers RBC injury, neutrophil activation, and macrophage remodeling as complementary components of a redox-inflammatory network linking microcirculatory alterations with innate immune responses. A focused, iterative search of PubMed, Scopus, Web of Science, and eLibrary.ru was used to identify relevant original and review articles. Oxidative and inflammatory stimuli remodel cell membranes and cytoskeletons and alter deformability, stiffness, adhesion, and migratory behavior. RBC adaptation to blood flow is closely linked to the maintenance of reversible deformability. Damaging factors, including prolonged storage, free iron, hemin, and oxidants, alter cell morphology, increase stiffness, and impair microcirculation. Hemolysis and the subsequent release of free iron and hemin further intensify oxidative damage to cell membranes. In neutrophils, priming, activation, and systemic inflammation induce changes in cell shape and physical properties, affecting capillary transit, tissue migration, and the propensity for NETosis. These alterations are associated with the severity of the inflammatory response. In macrophages, activation comprises a continuum of context-dependent functional states rather than two strictly separated M1 and M2 phenotypes. IRF5 regulates pro-inflammatory macrophage programs and represents a potential therapeutic target, although most evidence remains preclinical. The biomechanical parameters reviewed here should be considered experimental readouts or candidate biomarkers rather than clinically validated biomarkers. Their clinical translation requires method-specific standardization, independent reproducibility, and prospective validation.
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BibTeX
@article{sergunova2026biomechanics,
title = {{Biomechanics of Red Blood Cells, Neutrophils, and Macrophages Under Oxidative Stress and Inflammation: A Narrative Review.}},
author = {Viktoria Sergunova and Vera Shashkovskaya and Snezhanna Kandrashina and Mikhail Shvedov and Vladimir Inozemtsev and Ekaterina Sherstyukova},
journal = {Biology},
year = {2026},
month = sep,
doi = {10.3390/biology15191710},
url = {https://europepmc.org/article/MED/42883383},
note = {CC BY},
}
RIS
TY - JOUR
TI - Biomechanics of Red Blood Cells, Neutrophils, and Macrophages Under Oxidative Stress and Inflammation: A Narrative Review.
AU - Viktoria Sergunova
AU - Vera Shashkovskaya
AU - Snezhanna Kandrashina
AU - Mikhail Shvedov
AU - Vladimir Inozemtsev
AU - Ekaterina Sherstyukova
PY - 2026
DA - 2026/09/25
JO - Biology
DO - 10.3390/biology15191710
UR - https://europepmc.org/article/MED/42883383
AB - This narrative review summarizes current findings on the biomechanics of red blood cells (RBCs), neutrophils, and macrophages under oxidative stress and inflammation. Its cross-cell framework considers RBC injury, neutrophil activation, and macrophage remodeling as complementary components of a redox-inflammatory network linking microcirculatory alterations with innate immune responses. A focused, iterative search of PubMed, Scopus, Web of Science, and eLibrary.ru was used to identify relevant original and review articles. Oxidative and inflammatory stimuli remodel cell membranes and cytoskeletons and alter deformability, stiffness, adhesion, and migratory behavior. RBC adaptation to blood flow is closely linked to the maintenance of reversible deformability. Damaging factors, including prolonged storage, free iron, hemin, and oxidants, alter cell morphology, increase stiffness, and impair microcirculation. Hemolysis and the subsequent release of free iron and hemin further intensify oxidative damage to cell membranes. In neutrophils, priming, activation, and systemic inflammation induce changes in cell shape and physical properties, affecting capillary transit, tissue migration, and the propensity for NETosis. These alterations are associated with the severity of the inflammatory response. In macrophages, activation comprises a continuum of context-dependent functional states rather than two strictly separated M1 and M2 phenotypes. IRF5 regulates pro-inflammatory macrophage programs and represents a potential therapeutic target, although most evidence remains preclinical. The biomechanical parameters reviewed here should be considered experimental readouts or candidate biomarkers rather than clinically validated biomarkers. Their clinical translation requires method-specific standardization, independent reproducibility, and prospective validation.
SN - 2079-7737
ER -