ReviewHamostaseologie2017
New findings on venous thrombogenesis.
Review in Hamostaseologie, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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.
Who cites it
25 citing papers in PubMed, 65 citations in OpenAlex.
- Assessment of Hypercoagulability After Orthopedic Trauma Surgery Using Coagulation Biomarkers and TEG/ROTEM.International journal of molecular sciences · 2026Review
- Correlation between calcium levels and coronary microvascular disease in high-altitude environments: nested case-control study.Frontiers in cardiovascular medicine · 2026Article
- Review
- Are Gamers Prone to eThrombosis during Long Gaming Sessions?Life (Basel, Switzerland) · 2024Article
- Composition of thrombi in zebrafish: similarities and distinctions with mammals.Journal of thrombosis and haemostasis : JTH · 2024Article
- Extracellular vesicles in venous thromboembolism and pulmonary hypertension.Journal of nanobiotechnology · 2023Review
- Immune cell-mediated venous thrombus resolution.Research and practice in thrombosis and haemostasis · 2023Review
- Massive DVT from the proximal IVC to the pedal vein: Our approach using aspiration mechanical thrombectomy and open surgery thrombectomy.Radiology case reports · 2023Article
- Pulmonary artery embolism: comprehensive transcriptomic analysis in understanding the pathogenic mechanisms of the disease.BMC genomics · 2023Article
- A combination of strongly associated prothrombotic single nucleotide polymorphisms could efficiently predict venous thrombosis risk.Frontiers in cardiovascular medicine · 2023Article
- Article
- Haemostatic differences between SARS-CoV-2 PCR-positive and negative patients at the time of hospital admission.PloS one · 2022Article
- A case-control study on factor V Leiden: an independent, gender-dependent risk factor for venous thromboembolism.Thrombosis journal · 2021Article
- Article
- Aqueous extract of Whitmania pigra Whitman ameliorates ferric chloride-induced venous thrombosis in rats via antioxidation.Journal of thrombosis and thrombolysis · 2021Article
- ACE2: the molecular doorway to SARS-CoV-2.Cell & bioscience · 2020Review
- Dectin-1 and TIM3 Expression in Deep Vein Thrombosis of Lower Limbs (DVTLL).Journal of clinical medicine · 2020Article
- The need to manage the risk of thromboembolism in COVID-19 patients.Journal of vascular surgery · 2020Article
- Sickle Cell Disease: A Paradigm for Venous Thrombosis Pathophysiology.International journal of molecular sciences · 2020Review
- Cardiovascular resistance to thrombosis in 13-lined ground squirrels.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Venous thrombosis (VT) is the third most common cause of cardiovascular death worldwide. Complications from VT and pulmonary embolism are the leading cause of lost disability-adjusted life years. Risks include genetic (e.g., non-O blood group, activated protein C resistance, hyperprothrombinemia) and acquired (e.g., age, surgery, cancer, pregnancy, immobilisation, female hormone use) factors. Pathophysiologic mechanisms that promote VT are incompletely understood, but involve abnormalities in blood coagulability, vessel function, and flow (so-called Virchow's Triad). Epidemiologic studies of humans, animal models, and biochemical and biophysical investigations have revealed contributions from extrinsic, intrinsic, and common pathways of coagulation, endothelial cells, leukocytes, red blood cells, platelets, cell-derived microvesicles, stasis-induced changes in vascular cells, and blood rheology. Knowledge of these mechanisms may yield new therapeutic targets. Characterisation of mechanisms that mediate VT formation and stability, particularly in aging, are needed to advance understanding of VT.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.