Evidence map›Paper›PMID 42866340›Full record

ReviewFrontiers in immunology2026

Thrombocytopenia: from physiological homeostasis imbalance to mechanism-driven precision diagnosis and therapy.

Yuting Pan, Dan Yao, Miaoya Le, Zhengwei Tan, Jingjing Liu, Jing Ni, Zhiyan Chen, Baodong Ye

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Yuting PanDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Dan YaoXiangshan Hospital of TCM Medical and Health Group, Ningbo, China.
Miaoya LeDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Zhengwei TanDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Jingjing LiuDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Jing NiDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Zhiyan ChenLaboratory of Integrated Traditional Chinese and Western Medicine for Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, Zhejiang, China.
Baodong YeDepartment of Hematology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thrombocytopenia is not a monolithic disease but a common final pathway of disrupted platelet homeostasis spanning production, clearance, and distribution. The traditional count-centric paradigm, relying on empirical transfusion or steroid administration, frequently obscures underlying mechanistic drivers. This review advances a framework progressing from physiological homeostasis imbalance through pathological mechanisms to precision diagnosis and therapy. Recognizing that immune-targeted therapies are only appropriate when cytopenia is genuinely immune-mediated, we systematically deconstruct both immune and non-immune mechanisms to enable accurate etiological anchoring and avoid inappropriate immunomodulation. We systematically deconstruct the multidimensional pathogenesis along five axes: impaired production, immune-mediated destruction, distributional abnormality, consumptive loss, and pseudothrombocytopenia. Key molecular insights include megakaryocyte transcriptional governance (GATA-1, FLI-1, RUNX1), the platelet desialylation-Ashwell-Morell receptor clearance axis, complement cascade activation, and FcRn-mediated IgG homeostasis. Building on this mechanistic foundation, we propose a three-stage diagnostic algorithm: artifact exclusion, mechanistic localization via non-invasive biomarkers (IPF, TPO, autoantibodies), and etiological anchoring. In the therapeutic landscape, Thrombopoietin receptor agonists (TPO-RAs), FcRn antagonists (efgartigimod and rozanolixizumab), BTK inhibitors (rilzabrutinib), and Syk inhibitors have reshaped ITP management, while complement pathway inhibition (eculizumab, ravulizumab, narsoplimab) has transformed thrombotic microangiopathy outcomes.We posit that thrombocytopenia management has entered the precision medicine era; nevertheless, dynamic biomarker development for refractory cases, artificial intelligence-assisted decision-making, and interdisciplinary integration remain pressing frontiers.

Indexed as

Blood PlateletsHomeostasisThrombocytopeniaAnimalsBiomarkersHumansMegakaryocytesPrecision MedicineBiomarkersimmune thrombocytopeniaprecision medicinethrombocytopeniathrombotic microangiopathyTPO receptor agonist

Identifiers

PMID42866340
PMCPMC13656083

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Registered trials

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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.