ReviewJournal of artificial organs : the official journal of the Japanese Society for Artificial Organs2025
Key markers and detection methods for evaluating platelet dysfunction in mechanical circulatory support devices.
Review in Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- From biomimicry to clinical actionability: rethinking high-shear thrombosis as a mechanobiological system.Current opinion in hematology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Mechanical circulatory support devices (MCSDs) have emerged as life-saving interventions for patients with end-stage heart failure. However, the non-physiological shear stress (NPSS) generated by MCSDs is a known precipitant of platelet dysfunction, augmenting risks of thrombotic and bleeding complications. Addressing this issue necessitates innovative approaches to attenuate platelet dysfunction, thereby enhancing the safety of MCSDs. This review synthesizes knowledge pertaining to the normal hemostatic process, the implications of NPSS on platelet function, the array of markers extensively employed to assess platelet dysfunction, and relevant detection assays, within the scope of MCSDs-related hemocompatibility. NPSS can induce platelet activation and receptor shedding, causing both thrombosis and bleeding. The use of fluorescence-activated cell sorting (FACS) to monitor changes in markers, including platelet surface receptors, P-selectin, platelet monocyte aggregation (PMA), platelet-derived microparticles (PDMPs), and phosphatidylserine (PS), Enzyme-Linked Immunosorbent Assay (ELISA) for platelet secretion analysis, and the modified prothrombinase platelet activity state (PAS) for thrombin assessment, are central to investigating these consequences. PS and thrombin, particularly, present unique responses to NPSS, underscoring their potential as targeted markers for platelet dysfunction research. Additionally, assessments of morphological shifts and platelet aggregation, through scanning electron microscopy (SEM) and fluorescence microscopy provide a more visualized evaluation of NPSS-mediated platelet dysfunction. Combining distinct markers and assays is essential to understanding and potentially mitigating NPSS-induced complications in MCSD therapy. Future research should focus on validating NPSS-specific biomarkers, standardizing detection methodologies, and elucidating interactions with MCSD-induced hemolysis and coagulopathy, ultimately improving safety and efficacy.
Indexed as
Identifiers
40730707What 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.