Evidence map›Paper›PMID 41800098›Full record

ArticleFrontiers in pharmacology2026

Role of albumin in regulating platelet function.

Qiwen Tai, Mengnan Yang, Shuang Chen, Yue Xia, Chenglin Sun, Lili Zhao, Kangxi Zhou, Pixia Gong, Jie Shen, Qiuxia Huang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Article
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

14 authors.

Qiwen Tai *Jiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Mengnan Yang *Jiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Shuang ChenDepartment of Pathology and Pathophysiology and Bone Marrow, Transplantation Center of the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yue XiaJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Chenglin SunJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Lili ZhaoJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Kangxi ZhouJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Pixia GongJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Jie ShenJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Qiuxia HuangJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Qing LiJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Renping HuJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Rong YanJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.
Kesheng DaiJiangsu Institute of Hematology, the First Affiliated Hospital of Soochow University, NHC Key Laboratory of Thrombosis and Hemostasis, National Clinical Research Center for Hematologic, Suzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Hypoproteinemia, which occurs in diverse clinical conditions, can cause a range of complications such as thrombosis, which is among the most serious and potentially life-threatening. Albumin is a widely utilized clinical therapeutic agent; however, research regarding its regulatory effects on thrombosis remains limited, and existing clinical evidence presents conflicting findings. The precise mechanisms whereby albumin affects platelet thrombus formation require further investigation. Methods: After co-incubating albumin with platelets, various platelet function experiments were carried out. The participation of signaling pathways and protein structures in the mechanism was verified by means of Western blot technology, protein charge neutralization, and over expression of molecules. Validation was also conducted through the construction of animal models. Results: Albumin significantly inhibited platelet thrombus formation in a murine model of hypoproteinemia without inducing hemorrhagic risk. Platelet aggregation, integrin activation on the membrane surface, and ATP release induced by various agonists were all inhibited. Transmission electron microscopy and fluorescence confocal microscopy revealed that albumin could suppress granule release, alter granule distribution within platelets, and inhibit platelet spreading. Furthermore, albumin was found to reduce the phosphorylation levels of PKC and Akt in the platelet activation signaling pathway. By neutralizing the surface negative charge of albumin and adding cationic surfactants such as quaternary ammonium salts, we confirmed that the surface negative charge of albumin was critical to the inhibition of platelet aggregation and granule release. Conclusion: Albumin can inhibit platelet activation and thrombus formation through the negatively charged surface residues and by modulating the PKC and Akt signaling pathways.

Indexed as

albuminhypoproteinemiaplatelet activationsignal transduction pathwaythrombus

Identifiers

PMID41800098
PMCPMC12962907

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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.