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: 3 complete abstracts (735 words), 9 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 process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. erythrocyte aggregation), and the process of blood coagulation.
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: Hemostases.
Where it fits in the MeSH classification
- Broader topics
- Blood Physiological Phenomena
- Narrower topics
- Blood Coagulation; Platelet Activation
Related concepts
- Blood
- Erythrocyte Aggregation
- Blood Coagulation
Research landscape
PubMed indexes 125,955 records tagged with the MeSH heading “Hemostasis” (counts retrieved 2026-10-31). 12,558 of them (10.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 68,250 records.
Reviews account for 16,522 records (13.1%) and meta-analyses for 324. Randomized controlled trials number 4,353 (3.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 68,250 |
| 2000-2009 | 20,634 |
| 2010-2019 | 24,513 |
| 2020 onward | 12,558 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 16,522 | 13.1% |
| Meta-analyses | 324 | 0.3% |
| Randomized controlled trials | 4,353 | 3.5% |
Method: PubMed query "Hemostasis"[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 |
|---|---|---|---|---|
| SARS-CoV-2 Spike Protein Amyloid Fibrils Impair Fibrin Formation and Fibrinolysis | 2025 | Research article Design not recorded in structured metadata | 11 | cc by PMID 41295749 · DOI · PMC12713721 |
| Explainable AI unravels sepsis heterogeneity via coagulation-inflammation profiles for prognosis and stratification | 2025 | Research article Design not recorded in structured metadata | 10 | cc by PMID 41285832 · DOI · PMC12644763 |
| Platelet activation, aspirin, and cancer: From basic science to clinical trials | 2026 | Review article Design not recorded in structured metadata | 10 | cc by PMID 41592353 · DOI · PMC7619208 |
SARS-CoV-2 Spike Protein Amyloid Fibrils Impair Fibrin Formation and Fibrinolysis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Long COVID, or postacute sequelae of COVID-19 from SARS-CoV-2 infection, is a persistent debilitating disease affecting multiple systems and organs.
- Closing excerpt
- Our study proposes a molecular mechanism for how the Spike protein of SARS-CoV-2 could contribute to the formation of fibrinolysis-resistant microclots observed in long COVID.
- 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)
Long COVID, or postacute sequelae of COVID-19 from SARS-CoV-2 infection, is a persistent debilitating disease affecting multiple systems and organs. Long COVID pathophysiology is a complex and not fully established process. One prevailing theory is that the formation of fibrin amyloid microclots (fibrinaloids), due to SARS-CoV-2 infection, can induce persistent inflammation and capillary blockage. An association between the amyloidogenic Spike protein of SARS-CoV-2 and impaired fibrinolysis was made when it was observed that fibrin clots formed in the presence of a mixture of amyloid fibrils from the spike protein mediated resistance to plasmin lysis. Here, we use purified components from the coagulation cascade to investigate the molecular processes of impaired fibrinolysis using seven amyloidogenic SARS-COV-2 Spike peptides. Five of seven Spike amyloid fibrils appeared not to substantially interfere with the fibrinogen-fibrin-fibrinolysis process in vitro, while two spike fibrils were active in different ways. Spike601 amyloid fibrils (sequence 601-620) impaired thrombin-mediated fibrin formation by binding and sequestering fibrinogen but did not affect fibrinolysis. On the contrary, fibrin clots formed in the presence of Spike685 amyloid fibrils (sequence 685-701) exhibited a marked resistance to plasmin-mediated fibrinolysis. We conclude that Spike685 amyloid fibrils can induce dense fibrin clot networks as well as incorporate fibrin into aggregated structures that resist fibrinolysis. Our study proposes a molecular mechanism for how the Spike protein of SARS-CoV-2 could contribute to the formation of fibrinolysis-resistant microclots observed in long COVID.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41295749 · DOI · PMC12713721
Explainable AI unravels sepsis heterogeneity via coagulation-inflammation profiles for prognosis and stratification [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Sepsis is a leading cause of hospital mortality, and its significant heterogeneity complicates prognosis and stratification.
- Closing excerpt
- Our work, therefore, offers a set of simple, real-time executable tools for sepsis heterogeneity, demonstrating the potential to enhance sepsis clinical practice globally, particularly in resource-constrained healthcare settings.
- 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 (146 words)
Sepsis is a leading cause of hospital mortality, and its significant heterogeneity complicates prognosis and stratification. To address this challenge, we developed an explainable artificial intelligence prognostic model (SepsisFormer, a transformer-based neural network) and an automated risk-stratification tool (SMART) for sepsis. In a multi-center retrospective study of 12,408 sepsis patients, SepsisFormer achieved high predictive accuracy (AUC: 0.9301, sensitivity: 0.9346, and specificity: 0.8312). SMART (AUC: 0.7360) surpassed most established scoring systems. Seven coagulation-inflammatory routine laboratory measurements and patient age were identified to classify patients' four risk levels (mild, moderate, severe, dangerous) and two subphenotypes (CIS1 and CIS2), each with distinct clinical characteristics and mortality rates. Notably, patients with moderate/severe levels or CIS2 derive more significant benefits from anticoagulant treatment. Our work, therefore, offers a set of simple, real-time executable tools for sepsis heterogeneity, demonstrating the potential to enhance sepsis clinical practice globally, particularly in resource-constrained healthcare settings.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41285832 · DOI · PMC12644763
Platelet activation, aspirin, and cancer: From basic science to clinical trials [3]
Abstract reading summary — source excerpts
- Opening excerpt
- There is extensive evidence that aspirin prevents cancer, but the mechanism of action is uncertain.
- Closing excerpt
- Although thromboxane A2-dependent platelet activation is the most thoroughly investigated mechanism and the established drug target of the antiplatelet effect of low-dose aspirin, it seems biologically plausible that other pathways of platelet activation, such as the ADP-P2Y12 pathway, may play a similar and possibly complementary role.
- 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 (357 words)
There is extensive evidence that aspirin prevents cancer, but the mechanism of action is uncertain. Once-daily low-dose aspirin (75-100 mg) completely and permanently inactivates the cyclooxygenase (COX) activity of prostaglandin G/H synthase-1 (COX-1) in platelets, suppressing thromboxane (TX)A2-dependent platelet activation. In this article, we review the mechanistic links between platelet activation, inflammation, cancer development, and progression and summarize recent clinical trial results and associated biomarker studies. We hypothesize that persistently enhanced platelet activation has 2 distinct tumorigenic consequences mediated by the release of TXA2: (1) at sites of gastrointestinal mucosal lesions, it promotes a local inflammatory response with COX-2 induction and enhanced prostaglandin E2 biosynthesis, contributing to early events in carcinogenesis; (2) it inhibits T-cell immunity to cancer by the activation of TXA2 receptors in lymphocytes, promoting cancer progression and metastasis dissemination. Supporting these hypotheses, abnormal and persistent platelet activation has been demonstrated in patients recently diagnosed with cancer and in those with adenomatous colonic polyps. To date, most clinical trials evaluating aspirin have focused on either primary cancer prevention, metastasis prevention (adjuvant treatment), or cardiovascular prevention. For an individual, benefits may accrue from one (or all) of these areas, and they collectively need to be balanced against bleeding risk. Collating large clinical datasets for meta-analysis alongside mechanistic studies will inform the interpretation of clinical trials, with the aim of identifying individuals most likely to benefit from aspirin. SIGNIFICANCE STATEMENT: We reviewed the experimental and clinical evidence supporting a previously unrecognized role of platelet activation in both the early stage of colorectal carcinogenesis and in cancer progression and metastasis. The findings support the use of low-dose aspirin in cancer prevention and treatment. Data from large randomized clinical trials support the use of aspirin for the prevention of Lynch syndrome cancers and in the adjuvant setting for patients with colorectal cancer whose tumors have a mutation in the phosphatidylinositol 3-kinase pathway genes. Although thromboxane A2-dependent platelet activation is the most thoroughly investigated mechanism and the established drug target of the antiplatelet effect of low-dose aspirin, it seems biologically plausible that other pathways of platelet activation, such as the ADP-P2Y12 pathway, may play a similar and possibly complementary role.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41592353 · DOI · PMC7619208
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 CYP2C19 genotype, clopidogrel metabolism, platelet function, and cardiovascular events: a systematic review and meta-analysis [4]
- Research article Thrombosis risk associated with COVID-19 infection. A scoping review [5]
- Research article Efficacy and safety of anticoagulant therapy in three specific populations with sepsis: a meta-analysis of randomized controlled trials [6]
- Research article Association between statin use and plasma D-dimer levels. A systematic review and meta-analysis of randomised controlled trials [7]
- Research article Prognostic significance of high on-clopidogrel platelet reactivity after percutaneous coronary intervention: systematic review and meta-analysis [8]
- Research article The HAS-BLED Score for Predicting Major Bleeding Risk in Anticoagulated Patients With Atrial Fibrillation: A Systematic Review and Meta-analysis [9]
References
- Westman H, Hammarström P, Nyström S. SARS-CoV-2 Spike Protein Amyloid Fibrils Impair Fibrin Formation and Fibrinolysis. . 2025. PMID 41295749 · DOI · PMC12713721
- Zhu L, Chen Z, Zhang H, Chen H, Liu L, Yu W, et al.. Explainable AI unravels sepsis heterogeneity via coagulation-inflammation profiles for prognosis and stratification. . 2025. PMID 41285832 · DOI · PMC12644763
- Patrono C, Burn J, Patrignani P, Langley RE. Platelet activation, aspirin, and cancer: From basic science to clinical trials. . 2026. PMID 41592353 · DOI · PMC7619208
- Holmes MV, Perel P, Shah T, Hingorani AD, Casas JP. CYP2C19 genotype, clopidogrel metabolism, platelet function, and cardiovascular events: a systematic review and meta-analysis. JAMA. 2011. PMID 22203539 · DOI
- Al-Ani F, Chehade S, Lazo-Langner A. Thrombosis risk associated with COVID-19 infection. A scoping review. Thromb Res. 2020. PMID 32485418 · DOI · PMC7255332
- Umemura Y, Yamakawa K, Ogura H, Yuhara H, Fujimi S. Efficacy and safety of anticoagulant therapy in three specific populations with sepsis: a meta-analysis of randomized controlled trials. J Thromb Haemost. 2016. PMID 26670422 · DOI
- Sahebkar A, Serban C, Mikhailidis DP, Undas A, Lip GY, Muntner P, et al.. Association between statin use and plasma D-dimer levels. A systematic review and meta-analysis of randomised controlled trials. Thromb Haemost. 2015. PMID 26017749 · DOI
- Aradi D, Komócsi A, Vorobcsuk A, Rideg O, Tokés-Füzesi M, Magyarlaki T, et al.. Prognostic significance of high on-clopidogrel platelet reactivity after percutaneous coronary intervention: systematic review and meta-analysis. Am Heart J. 2010. PMID 20826265 · DOI
- Zhu W, He W, Guo L, Wang X, Hong K. The HAS-BLED Score for Predicting Major Bleeding Risk in Anticoagulated Patients With Atrial Fibrillation: A Systematic Review and Meta-analysis. Clin Cardiol. 2015. PMID 26418409 · DOI · PMC6490831
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.