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 (761 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
The destruction of erythrocytes by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.
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: Haemolysis; Haemolyses; Intravascular Hemolysis; Hemolyses, Intravascular; Hemolysis, Intravascular; Intravascular Hemolyses; Extravascular Hemolysis; Extravascular Hemolyses.
Where it fits in the MeSH classification
- Broader topics
- Pathologic Processes; Antigen-Antibody Reactions
- See also
- Anemia, Hemolytic; Osmotic Fragility
Related concepts
Research landscape
PubMed indexes 33,070 records tagged with the MeSH heading “Hemolysis” (counts retrieved 2026-10-29). 3,929 of them (11.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 18,283 records.
Reviews account for 1,576 records (4.8%) and meta-analyses for 24. Randomized controlled trials number 206 (0.6%) 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 | 18,283 |
| 2000-2009 | 4,287 |
| 2010-2019 | 6,571 |
| 2020 onward | 3,929 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,576 | 4.8% |
| Meta-analyses | 24 | 0.1% |
| Randomized controlled trials | 206 | 0.6% |
Method: PubMed query "Hemolysis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
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 |
|---|---|---|---|---|
| Optimization of the Hemolysis Assay for the Assessment of Cytotoxicity | 2023 | Research article Design not recorded in structured metadata | 306 | cc by PMID 36769243 · DOI · PMC9917735 |
| Hemolysis contributes to anemia during long-duration space flight | 2022 | Research article Design not recorded in structured metadata | 69 | cc by PMID 35031790 · DOI · PMC8799460 |
| The lexicon of antimicrobial peptides: a complete set of arginine and tryptophan sequences | 2021 | Research article Design not recorded in structured metadata | 69 | cc by PMID 34021253 · DOI · PMC8140080 |
| Novel ABCG5 and ABCG8 Variants in Sitosterolemia: Insights Into Haemolysis, Calcium Dysregulation and Therapeutic Challenges | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42111500 · DOI · PMC13157300 |
Optimization of the Hemolysis Assay for the Assessment of Cytotoxicity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- In vitro determination of hemolytic properties is a common and important method for preliminary evaluation of cytotoxicity of chemicals, drugs, or any blood-contacting medical device or material.
- Closing excerpt
- Based on our findings we propose an optimized protocol in an attempt to standardize future hemolysis studies.
- 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 (181 words)
In vitro determination of hemolytic properties is a common and important method for preliminary evaluation of cytotoxicity of chemicals, drugs, or any blood-contacting medical device or material. The method itself is relatively straightforward, however, protocols used in the literature vary substantially. This leads to significant difficulties both in interpreting and in comparing the obtained values. Here, we examine how the different variables used under different experimental setups may affect the outcome of this assay. We find that certain key parameters affect the hemolysis measurements in a critical manner. The hemolytic effect of compounds tested here varied up to fourfold depending on the species of the blood source. The use of different types of detergents used for generating positive control samples (i.e., 100% hemolysis) produced up to 2.7-fold differences in the calculated hemolysis ratios. Furthermore, we find an expected, but substantial, increase in the number of hemolyzed erythrocytes with increasing erythrocyte concentration and with prolonged incubation time, which in turn affects the calculated hemolysis ratios. Based on our findings we propose an optimized protocol in an attempt to standardize future hemolysis studies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36769243 · DOI · PMC9917735
Hemolysis contributes to anemia during long-duration space flight [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Anemia in astronauts has been noted since the first space missions, but the mechanisms contributing to anemia in space flight have remained unclear.
- Closing excerpt
- These findings suggest that the destruction of red blood cells, termed hemolysis, is a primary effect of microgravity in space flight and support the hypothesis that the anemia associated with space flight is a hemolytic condition that should be considered in the screening and monitoring of both astronauts and space tourists.
- 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 (127 words)
Anemia in astronauts has been noted since the first space missions, but the mechanisms contributing to anemia in space flight have remained unclear. Here, we show that space flight is associated with persistently increased levels of products of hemoglobin degradation, carbon monoxide in alveolar air and iron in serum, in 14 astronauts throughout their 6-month missions onboard the International Space Station. One year after landing, erythrocytic effects persisted, including increased levels of hemolysis, reticulocytosis and hemoglobin. These findings suggest that the destruction of red blood cells, termed hemolysis, is a primary effect of microgravity in space flight and support the hypothesis that the anemia associated with space flight is a hemolytic condition that should be considered in the screening and monitoring of both astronauts and space tourists.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35031790 · DOI · PMC8799460
The lexicon of antimicrobial peptides: a complete set of arginine and tryptophan sequences [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Our understanding of the activity of cationic antimicrobial peptides (AMPs) has focused on well-characterized natural sequences, or limited sets of synthetic peptides designed de novo.
- Closing excerpt
- The maximum specific antimicrobial activity appeared to occur in peptides of around 10 residues, suggesting 'diminishing returns' for developing larger peptides, when activity is considered per residue of peptide.
- 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 (198 words)
Our understanding of the activity of cationic antimicrobial peptides (AMPs) has focused on well-characterized natural sequences, or limited sets of synthetic peptides designed de novo. We have undertaken a comprehensive investigation of the underlying primary structural features that give rise to the development of activity in AMPs. We consider a complete set of all possible peptides, up to 7 residues long, composed of positively charged arginine (R) and / or hydrophobic tryptophan (W), two features most commonly associated with activity. We found the shortest active peptides were 4 or 5 residues in length, and the overall landscapes of activity against gram-positive and gram-negative bacteria and a yeast were positively correlated. For all three organisms we found a single activity peak corresponding to sequences with around 40% R; the presence of adjacent W duplets and triplets also conferred greater activity. The mechanistic basis of these activities comprises a combination of lipid binding, particularly to negatively charged membranes, and additionally peptide aggregation, a mode of action previously uninvestigated for such peptides. The maximum specific antimicrobial activity appeared to occur in peptides of around 10 residues, suggesting 'diminishing returns' for developing larger peptides, when activity is considered per residue of peptide.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34021253 · DOI · PMC8140080
Novel ABCG5 and ABCG8 Variants in Sitosterolemia: Insights Into Haemolysis, Calcium Dysregulation and Therapeutic Challenges [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Sitosterolemia is a rare autosomal recessive lipid metabolic disorder caused by mutations in ABCG5 or ABCG8, leading to pathological accumulation of dietary plant sterols.
- Closing excerpt
- Our findings indicate that combining ezetimibe with Ca2+-modulating therapy may represent a novel strategy to reduce haemolysis in sitosterolemia.
- 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 (255 words)
Sitosterolemia is a rare autosomal recessive lipid metabolic disorder caused by mutations in ABCG5 or ABCG8, leading to pathological accumulation of dietary plant sterols. The condition is clinically heterogeneous, presenting with xanthomas, premature atherosclerosis and haematological abnormalities such as stomatocytosis, haemolytic anaemia and thrombocytopenia, making diagnosis particularly challenging. We investigated four patients with unexplained inherited haemolytic anaemia and a history of recurrent transfusions to identify molecular and functional mechanisms and explore therapeutic options. Haematological work-up, including CBC, peripheral smear, reticulocyte count, EMA binding assay, red cell enzyme activity and HPLC for haemoglobinopathies, was performed, along with biochemical assays for liver, renal and lipid function. Plasma sterol levels were quantified using GC-MS, whereas functional assays included intracellular calcium flux under osmotic stress, red cell density profiling and ROS measurement. Whole-exome sequencing identified homozygous nonsense variants: a novel ABCG8 (p.Trp584∗) in two siblings, ABCG5 (p.Arg243∗) in one patient and ABCG8 (p.Ser129∗) in another. Two patients showed markedly elevated plasma phytosterols, predominantly stigmasterol and β-sitosterol. Ezetimibe therapy (10 mg/day for 6 months) effectively reduced sterol levels but failed to normalise haemoglobin or significantly reduce overhydrated red cell populations. Functional studies demonstrated elevated intracellular Ca2+, enhanced influx under stress, increased ROS and a persistent population of stomatocytes. In silico prediction tools confirmed the pathogenicity of the identified variants. Persistent haemolysis despite sterol-lowering therapy suggests irreversible red cell membrane damage due to sterol incorporation, altered fluidity, oxidative stress and calcium dysregulation. Our findings indicate that combining ezetimibe with Ca2+-modulating therapy may represent a novel strategy to reduce haemolysis in sitosterolemia.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42111500 · DOI · PMC13157300
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 The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease [5]
- Research article Hemolysis and free hemoglobin revisited: exploring hemoglobin and hemin scavengers as a novel class of therapeutic proteins [6]
- Research article Intravascular hemolysis and the pathophysiology of sickle cell disease [7]
- Research article Pathophysiology of Sickle Cell Disease [8]
- Research article Haemolysis: an overview of the leading cause of unsuitable specimens in clinical laboratories [9]
- Research article Red blood cell hemolysis during processing [10]
References
- Sæbø IP, Bjørås M, Franzyk H, Helgesen E, Booth JA. Optimization of the Hemolysis Assay for the Assessment of Cytotoxicity. . 2023. PMID 36769243 · DOI · PMC9917735
- Trudel G, Shahin N, Ramsay T, Laneuville O, Louati H. Hemolysis contributes to anemia during long-duration space flight. . 2022. PMID 35031790 · DOI · PMC8799460
- Clark S, Jowitt TA, Harris LK, Knight CG, Dobson CB. The lexicon of antimicrobial peptides: a complete set of arginine and tryptophan sequences. . 2021. PMID 34021253 · DOI · PMC8140080
- Warang P, Dongerdiye R, Dehadrai P, Kamble P, Samanpalliwar N, Madkaikar M, et al.. Novel ABCG5 and ABCG8 Variants in Sitosterolemia: Insights Into Haemolysis, Calcium Dysregulation and Therapeutic Challenges. . 2026. PMID 42111500 · DOI · PMC13157300
- Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. JAMA. 2005. PMID 15811985 · DOI
- Schaer DJ, Buehler PW, Alayash AI, Belcher JD, Vercellotti GM. Hemolysis and free hemoglobin revisited: exploring hemoglobin and hemin scavengers as a novel class of therapeutic proteins. Blood. 2013. PMID 23264591 · DOI · PMC3578950
- Kato GJ, Steinberg MH, Gladwin MT. Intravascular hemolysis and the pathophysiology of sickle cell disease. J Clin Invest. 2017. PMID 28248201 · DOI · PMC5330745
- Sundd P, Gladwin MT, Novelli EM. Pathophysiology of Sickle Cell Disease. Annu Rev Pathol. 2019. PMID 30332562 · DOI · PMC7053558
- Lippi G, Blanckaert N, Bonini P, Green S, Kitchen S, Palicka V, et al.. Haemolysis: an overview of the leading cause of unsuitable specimens in clinical laboratories. Clin Chem Lab Med. 2008. PMID 18601596 · DOI
- Sowemimo-Coker SO. Red blood cell hemolysis during processing. Transfus Med Rev. 2002. PMID 11788929 · DOI
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 2026-10-29.
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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.