Integrin αIIbβ3 Deficiency Impairs Platelet Formation Through Serine Metabolic Dysregulation in Megakaryocytes
Highlight
- Integrin αIIbβ3 deficiency in megakaryocytes leads to impaired platelet biogenesis, despite normal megakaryocyte differentiation.
- Deficiency or activating mutations in ITGB3 reduce proplatelet formation, demonstrating a quantitative role of integrin independent of mutation type.
- Transcriptomic and metabolomic analyses reveal disrupted serine metabolism linked to reduced expression of amino acid transporter CD98hc (SLC3A2) in integrin-deficient megakaryocytes.
- Reintroduction of wild-type ITGB3 restores αIIbβ3, CD98hc expression, serine uptake, and platelet formation, identifying a novel integrin-mediated metabolic regulation pathway in thrombopoiesis.
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This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.