Evidence map›Paper›PMID 28279217›Full record

ReviewCardiovascular diabetology2017

Hypofibrinolysis in diabetes: a therapeutic target for the reduction of cardiovascular risk.

Katherine Kearney, Darren Tomlinson, Kerrie Smith, Ramzi Ajjan

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cardiovascular diabetology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% of its field
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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
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  16. Atrial Cardiomyopathy: From Diagnosis to Treatment.Reviews in cardiovascular medicine · 2025
    Review
  17. Hyperglycemia and Venous Thromboembolism.Diagnostics (Basel, Switzerland) · 2024
    Review
  18. Review
  19. Review
  20. Review

4 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Katherine KearneyDivision of Cardiovascular & Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, LS2 9JT, UK.
Darren TomlinsonBiomedical Health Research Centre, Astbury Building, University of Leeds, Leeds, LS2 9JT, UK.
Kerrie SmithDivision of Cardiovascular & Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, LS2 9JT, UK.
Ramzi AjjanDivision of Cardiovascular & Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, LS2 9JT, UK. R.Ajjan@leeds.ac.uk.
University of Leeds · GB

Funding

British Heart Foundation FS/10/020/28242British Heart Foundation FS/15/40/31536
6 · The paper itself

Abstract

An enhanced thrombotic environment and premature atherosclerosis are key factors for the increased cardiovascular risk in diabetes. The occlusive vascular thrombus, formed secondary to interactions between platelets and coagulation proteins, is composed of a skeleton of fibrin fibres with cellular elements embedded in this network. Diabetes is characterised by quantitative and qualitative changes in coagulation proteins, which collectively increase resistance to fibrinolysis, consequently augmenting thrombosis risk. Current long-term therapies to prevent arterial occlusion in diabetes are focussed on anti-platelet agents, a strategy that fails to address the contribution of coagulation proteins to the enhanced thrombotic milieu. Moreover, antiplatelet treatment is associated with bleeding complications, particularly with newer agents and more aggressive combination therapies, questioning the safety of this approach. Therefore, to safely control thrombosis risk in diabetes, an alternative approach is required with the fibrin network representing a credible therapeutic target. In the current review, we address diabetes-specific mechanistic pathways responsible for hypofibrinolysis including the role of clot structure, defects in the fibrinolytic system and increased incorporation of anti-fibrinolytic proteins into the clot. Future anti-thrombotic therapeutic options are discussed with special emphasis on the potential advantages of modulating incorporation of the anti-fibrinolytic proteins into fibrin networks. This latter approach carries theoretical advantages, including specificity for diabetes, ability to target a particular protein with a possible favourable risk of bleeding. The development of alternative treatment strategies to better control residual thrombosis risk in diabetes will help to reduce vascular events, which remain the main cause of mortality in this condition.

Indexed as

AnimalsCardiovascular DiseasesDiabetes MellitusFibrinogenFibrinolysisFibrinolytic AgentsHemorrhageHumansPlatelet Aggregation InhibitorsRisk AssessmentRisk FactorsThrombosisFibrinogenFibrinolytic AgentsPlatelet Aggregation InhibitorsDiabetesFibrinogenFibrinolysis

Identifiers

PMID28279217
PMCPMC5345237
OpenAlexW2592424182

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.