Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (734 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Erythrocyte; Red Blood Cells; Blood Cell, Red; Red Blood Cell; Red Blood Corpuscles; Blood Corpuscle, Red; Red Blood Corpuscle; Blood Cells, Red.
Where it fits in the MeSH classification
- Broader topics
- Blood Cells; Erythroid Cells
- Narrower topics
- Erythrocyte Membrane; Erythrocytes, Abnormal; Reticulocytes; Erythroid Precursor Cells
Related concepts
- Hemoglobin
- Oxygen
Research landscape
PubMed indexes 182,613 records tagged with the MeSH heading “Erythrocytes” (counts retrieved 2026-10-31). 10,953 of them (6.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 120,171 records.
Reviews account for 8,499 records (4.7%) and meta-analyses for 120. Randomized controlled trials number 1,531 (0.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 120,171 |
| 2000-2009 | 25,122 |
| 2010-2019 | 26,367 |
| 2020 onward | 10,953 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,499 | 4.7% |
| Meta-analyses | 120 | 0.1% |
| Randomized controlled trials | 1,531 | 0.8% |
Method: PubMed query "Erythrocytes"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Dynamics of microcompartment formation at the mitosis-to-G1 transition | 2025 | Research article Design not recorded in structured metadata | 27 | cc by PMID 41107486 · DOI · PMC12700819 |
| RBC Membrane-Camouflaged Nanosystem-Mediated Synergistic Drug Combination for Enhanced Anti-Tumor Therapy | 2025 | Research article Design not recorded in structured metadata | 16 | cc by PMID 40331462 · DOI · PMC12506840 |
| RIFINs displayed on malaria-infected erythrocytes bind KIR2DL1 and KIR2DS1 | 2025 | Research article Design not recorded in structured metadata | 13 | cc by PMID 40500441 · DOI · PMC12310515 |
| PTRAMP, CSS and Ripr form a conserved complex required for merozoite invasion of Plasmodium species into erythrocytes | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41587959 · DOI · PMC12916814 |
Dynamics of microcompartment formation at the mitosis-to-G1 transition [1]
Abstract reading summary — source excerpts
- Opening excerpt
- As cells exit mitosis and enter G1, chromosomes decompact and transcription is reestablished.
- Closing excerpt
- Our results suggest that compaction and homotypic affinity drive microcompartment formation, which may explain transient transcriptional spiking at mitotic exit.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (153 words)
As cells exit mitosis and enter G1, chromosomes decompact and transcription is reestablished. Hi-C studies have indicated that all interphase three-dimensional genome features, including A/B compartments, topologically associating domains and CCCTC-binding factor loops, are lost during mitosis. However, Hi-C is insensitive to features such as microcompartments, nested focal interactions between cis-regulatory elements. Here we apply region capture Micro-C to mouse erythroblasts from mitosis to G1. We unexpectedly observe microcompartments in prometaphase, which strengthen in anaphase and telophase before weakening throughout G1. Microcompartment anchors coincide with transcriptionally spiking promoters during mitosis. Loss of condensin loop extrusion differentially impacts microcompartments and A/B compartments, suggesting that they are partially distinct. Polymer modeling shows that microcompartment formation is favored by chromatin compaction and disfavored by loop extrusion, providing a basis for strong microcompartmentalization in anaphase and telophase. Our results suggest that compaction and homotypic affinity drive microcompartment formation, which may explain transient transcriptional spiking at mitotic exit.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41107486 · DOI · PMC12700819
RBC Membrane-Camouflaged Nanosystem-Mediated Synergistic Drug Combination for Enhanced Anti-Tumor Therapy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Achieving direct delivery of drugs to the tumor site is a prerequisite for successful drug development, necessitating that drug molecules be cell permeable.
- Closing excerpt
- Overall, the biomimetic nanosystem realizes enhanced drug combination therapy with high-level biosafety, which provides a facile strategy to improve the clinical application of CPPs-based drug combinations.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (173 words)
Achieving direct delivery of drugs to the tumor site is a prerequisite for successful drug development, necessitating that drug molecules be cell permeable. Numerous studies have shown that cell-penetrating peptides (CPPs) can augment the efficacy of various therapeutic agents by enhancing cellular uptake, prompting their advancement into preclinical studies. However, the non-specificity and cationic properties of CPPs impede their clinical application. Attributed to the easily accessible capacity and excellent biocompatibility of red blood cells (RBC), herein, an RBC membrane camouflaged, cell-penetrating peptides R8-(RRRRRRRR)based drug delivery system is constructed to achieve a synergistic combination of natural compounds triptolide (TP) and celastrol (Cel), thus precisely inducing tumor inhibition. The RBC membrane camouflaged nanosystem escaped from the reticuloendothelial system (RES) and is endocytosed by tumor cells mediated by R8. Released TP and Cel-induced tumor cell apoptosis, reducing tumor metastasis invasion and triggering autophagy disorder in breast cancer and liver cancer. Overall, the biomimetic nanosystem realizes enhanced drug combination therapy with high-level biosafety, which provides a facile strategy to improve the clinical application of CPPs-based drug combinations.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40331462 · DOI · PMC12506840
RIFINs displayed on malaria-infected erythrocytes bind KIR2DL1 and KIR2DS1 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Natural killer (NK) cells use inhibitory and activating immune receptors to differentiate between human cells and pathogens.
- Closing excerpt
- This study demonstrates that activating killer immunoglobulin-like receptors can recruit NK cells to target a pathogen and reveals a potential role for activating immune receptors in controlling malaria infection.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (232 words)
Natural killer (NK) cells use inhibitory and activating immune receptors to differentiate between human cells and pathogens. Signalling by these receptors determines whether an NK cell becomes activated and destroys a target cell. In some cases, such as killer immunoglobulin-like receptors, immune receptors are found in pairs, with inhibitory and activating receptors containing nearly identical extracellular ligand-binding domains coupled to different intracellular signalling domains1. Previous studies showed that repetitive interspersed family (RIFIN) proteins, displayed on the surfaces of Plasmodium falciparum-infected erythrocytes, can bind to inhibitory immune receptors and dampen NK cell activation2,3, reducing parasite killing. However, no pathogen-derived ligand has been identified for any human activating receptor. Here we identified a clade of RIFINs that bind to inhibitory immune receptor KIR2DL1 more strongly than KIR2DL1 binds to the human ligand (MHC class I). This interaction mediates inhibitory signalling and suppresses the activation of KIR2DL1-expressing NK cells. We show that KIR2DL1-binding RIFINs are abundant in field-isolated strains from both Africa and Asia and reveal how the two RIFINs bind to KIR2DL1. The RIFIN binding surface of KIR2DL1 is conserved in the cognate activating immune receptor KIR2DS1. We find that KIR2DL1-binding RIFINs can also bind to KIR2DS1, resulting in the activation of KIR2DS1-expressing NK cells. This study demonstrates that activating killer immunoglobulin-like receptors can recruit NK cells to target a pathogen and reveals a potential role for activating immune receptors in controlling malaria infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40500441 · DOI · PMC12310515
PTRAMP, CSS and Ripr form a conserved complex required for merozoite invasion of Plasmodium species into erythrocytes [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Invasion of erythrocytes by members of the Plasmodium genus is an essential step of the parasite lifecycle, orchestrated by numerous host-parasite interactions.
- Closing excerpt
- with implications for vaccines targeting multiple species of malaria-causing parasites.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (176 words)
Invasion of erythrocytes by members of the Plasmodium genus is an essential step of the parasite lifecycle, orchestrated by numerous host-parasite interactions. In P. falciparum Rh5, with PfCyRPA, PfRipr, PfCSS, and PfPTRAMP, forms the essential PCRCR complex which binds basigin on the erythrocyte surface. Rh5 is restricted to P. falciparum and its close relatives; however, PTRAMP, CSS and Ripr orthologs are present across the Plasmodium genus. We investigated PTRAMP, CSS and Ripr orthologs from three species to elucidate common features of the complex. Like P. falciparum, PTRAMP and CSS form a disulfide-linked heterodimer in both P. vivax and P. knowlesi with all three species forming a complex with Ripr by binding its C-terminal region, termed the PTRAMP-CSS-Ripr (PCR) complex. Cross-reactive antibodies targeting the PCR complex differentially inhibit merozoite invasion. The crystal structure of a cross-reactive antibody reveals an inhibitory epitope on the C-terminal tail of PvRipr. Cryo-EM visualization of the P. knowlesi PCR complex confirms predicted models and demonstrates a core invasion scaffold in Plasmodium spp. with implications for vaccines targeting multiple species of malaria-causing parasites.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41587959 · DOI · PMC12916814
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Red blood cell storage lesion: causes and potential clinical consequences [5]
- Research article Living on the Edge: Efferocytosis at the Interface of Homeostasis and Pathology [6]
- Research article Red blood cells: the forgotten player in hemostasis and thrombosis [7]
- Research article Red cell distribution width and mortality in older adults: a meta-analysis [8]
- Research article Thrombus Structural Composition in Cardiovascular Disease [9]
- Research article Transfusion-related red blood cell alloantibodies: induction and consequences [10]
References
- Goel VY, Aboreden NG, Jusuf JM, Zhang H, Mori LP, Mirny LA, et al.. Dynamics of microcompartment formation at the mitosis-to-G1 transition. . 2025. PMID 41107486 · DOI · PMC12700819
- Cheng Q, Zhong X, Deng L, He X, Luo M, Wang R, et al.. RBC Membrane-Camouflaged Nanosystem-Mediated Synergistic Drug Combination for Enhanced Anti-Tumor Therapy. . 2025. PMID 40331462 · DOI · PMC12506840
- Sakoguchi A, Chamberlain SG, Mørch AM, Widdess M, Harrison TE, Dustin ML, et al.. RIFINs displayed on malaria-infected erythrocytes bind KIR2DL1 and KIR2DS1. . 2025. PMID 40500441 · DOI · PMC12310515
- Seager BA, Lim PS, Xiao X, Lai KH, Feufack-Donfack LB, Dass S, et al.. PTRAMP, CSS and Ripr form a conserved complex required for merozoite invasion of Plasmodium species into erythrocytes. . 2026. PMID 41587959 · DOI · PMC12916814
- Yoshida T, Prudent M, D'alessandro A. Red blood cell storage lesion: causes and potential clinical consequences. Blood Transfus. 2019. PMID 30653459 · DOI · PMC6343598
- Morioka S, Maueröder C, Ravichandran KS. Living on the Edge: Efferocytosis at the Interface of Homeostasis and Pathology. Immunity. 2019. PMID 31117011 · DOI · PMC6721617
- Weisel JW, Litvinov RI. Red blood cells: the forgotten player in hemostasis and thrombosis. J Thromb Haemost. 2019. PMID 30618125 · DOI · PMC6932746
- Patel KV, Semba RD, Ferrucci L, Newman AB, Fried LP, Wallace RB, et al.. Red cell distribution width and mortality in older adults: a meta-analysis. J Gerontol A Biol Sci Med Sci. 2010. PMID 19880817 · DOI · PMC2822283
- Alkarithi G, Duval C, Shi Y, Macrae FL, Ariëns RAS. Thrombus Structural Composition in Cardiovascular Disease. Arterioscler Thromb Vasc Biol. 2021. PMID 34261330 · DOI · PMC8384252
- Tormey CA, Hendrickson JE. Transfusion-related red blood cell alloantibodies: induction and consequences. Blood. 2019. PMID 30808636 · DOI · PMC6484385
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.