ArticleBiomarker research2025
Age- and sex-specific transcriptomic changes drive the prothrombotic potential of megakaryocytes.
Article in Biomarker research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Fibrin-Binding Peptide-Functionalized HBiomedicines · 2026Article
- Inherited Platelet GPIV Deficiency: First Description of a Series of Unrelated Patients with Bleeding Diathesis.Biomolecules · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Aging is associated with enhanced platelet activation and inflammatory responses, contributing to an increased risk of thrombotic and cardiovascular events. However, how megakaryocytes (Mk) change with age or between sexes is still unclear.We performed single-cell RNA sequencing to profile bone marrow from young (3-month-old) and old (> 24-month-old) C57BL/6 mice, as well as from young and middle-aged human donors. In parallel, platelet activation was assessed by CD62P expression using flow cytometry in isolated and washed mouse platelets from young and old donors. Single-cell clustering in mouse bone marrow revealed five distinct Mk subpopulations. The age-dependent shift was more pronounced for subpopulations associated with platelet activation (mMk3) and immune/inflammatory responses (mMk4). mMk3 cells were more abundant in females, whereas mMk4 predominated in males. An increased platelet activation phenotype in old mice was confirmed in both sexes by CD62P expression analyses. Differential gene expression analyses showed that aging alters gene expression patterns related to platelet activation and aggregation via receptor signaling, granule formation, and inflammation. Aged males exhibited enrichment in genes linked to mitochondrial function, oxidative stress, lipid metabolism and membrane dynamics, whereas aged females showed upregulation of serotonin receptor genes. Human transcriptomic data support our murine findings, exhibiting increased expression of genes involved in mitochondrial electron transport and immune signaling in middle-aged individuals. Our study reveals a complex, sex-specific remodeling of Mk subpopulations in the aging organisms, characterized by distinct pro-thrombotic and pro-inflammatory transcriptional profiles. These observations suggest potential targets for developing age- and sex-tailored antithrombotic therapies.
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.