Evidence map›Paper›PMID 39519000›Full record

ReviewInternational journal of molecular sciences2024

The Basic Principles of Pathophysiology of Venous Thrombosis.

Sam Schulman, Alexander Makatsariya, Jamilya Khizroeva, Victoria Bitsadze, Daredzhan Kapanadze

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. [Management of emergencies in rheumatology].Zeitschrift fur Rheumatologie · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. [Management of emergencies in rheumatology].Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Haemostasis and the Need for Antithrombotics: An Introduction.Handbook of experimental pharmacology · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Sam SchulmanDepartment of Medicine, Thrombosis and Atherosclerosis Research Institute, McMaster University, 1280 Main St W, Hamilton, ON L8S 4L8, Canada.ORCID 0000-0002-8512-9043
Alexander MakatsariyaDepartment of Obstetrics, Gynecology and Perinatal Medicine, The I.M. Sechenov First Moscow State Medical University (Sechenov University), Trubetskaya Str 8-2, 119435 Moscow, Russia.
Jamilya KhizroevaDepartment of Obstetrics, Gynecology and Perinatal Medicine, The I.M. Sechenov First Moscow State Medical University (Sechenov University), Trubetskaya Str 8-2, 119435 Moscow, Russia.ORCID 0000-0002-0725-9686
Victoria BitsadzeDepartment of Obstetrics, Gynecology and Perinatal Medicine, The I.M. Sechenov First Moscow State Medical University (Sechenov University), Trubetskaya Str 8-2, 119435 Moscow, Russia.
Daredzhan KapanadzeCenter of Pathology of Pregnancy and Hemostasis «Medlabi», Tbilisi 340112, Georgia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The past few decades have brought tremendous insight into the molecular and pathophysiological mechanisms responsible for thrombus generation. For a clinician, it is usually sufficient to explain the incident of deep vein thrombosis (DVT) with provoking factors such as trauma with vascular injury, immobilization, hormonal factors, or inherited or acquired coagulation defects. About half of DVTs are, however, lacking such triggers and are called unprovoked. Venous stasis and hypoxia at the valve sinus level may start a chain of reactions. The concept of immunothrombosis has added a new dimension to the old etiological triad of venous stasis, vessel wall injury, and changes in blood components. This is particularly important in COVID-19, where hyperinflammation, cytokines, and neutrophil extracellular traps are associated with the formation of microthrombi in the lungs. To better understand the mechanisms behind DVT and reach beyond the above-mentioned simplifications, animal models and clinical epidemiological studies have brought insight into the complex interplay between leukocytes, platelets, endothelium, cytokines, complements, and coagulation factors and inhibitors. These pathways and the interplay will be reviewed here, as well as the roles of cancer, anticancer drugs, and congenital thrombophilic defects on the molecular level in hypercoagulability and venous thromboembolism.

Indexed as

COVID-19Venous ThrombosisAnimalsBlood CoagulationBlood PlateletsCytokinesExtracellular TrapsHumansSARS-CoV-2Cytokinescomplementscytokineshypoxianeutrophil extracellular trapsstasisvenous thromboembolism

Identifiers

PMID39519000
PMCPMC11547114

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.