Platelets are the second most abundant cell type in blood and play an essential role in the immune response by orchestrating blood coagulation during wound healing (1). Because of their short life span of under 10 d, it is critical for the body to be able to constantly replenish platelets in the blood stream, and low platelet counts are indeed associated with a slew of pathologies with major health and economic consequences. Understanding the process of platelet biogenesis is thus paramount for the development of efficient in vivo therapies, as well as for the design of bioreactors capable of producing platelets in vitro (2) for subsequent transfusion. In PNAS, Bächer et al. (3) cast light on the fundamental biophysics of this process using a computational model of platelet formation that recapitulates the salient features of in vitro experiments. Their model points to a primarily physical mechanism for platelet biogenesis based on an interfacial instability triggered by adenosine 5′-triphosphate (ATP)-driven membrane stresses and demonstrates a strong acceleration of the rate of platelet production in the presence of an external fluid flow.

中文翻译：

---

血小板形成的物理机制。

血小板是血液中第二丰富的细胞类型，在伤口愈合过程中通过协调血液凝结，血小板在免疫反应中起重要作用（1）。由于它们的生命周期短于10 d，因此对于人体而言，不断补充血液中的血小板至关重要，而血小板数量低的确与一系列病理相关，对健康和经济造成重大影响。因此，了解血小板生物发生的过程对于开发有效的体内疗法以及设计能够在体外产生血小板以进行后续输血的生物反应器的设计至关重要（2）。在PNAS中，Bächer等人。（3）使用血小板形成的计算模型来概述该过程的基本生物物理学，该模型概括了体外实验的显着特征。他们的模型指出了基于由5'-三磷酸腺苷（ATP）驱动的膜应力触发的界面不稳定性的血小板生物发生的主要物理机制，并证明了在存在外部流体流的情况下，血小板产生速率的强烈加速。