Asaro Robert J, Cabrales Pedro
Department of Structural Engineering, University of California, San Diego, CA 92093, USA.
Department of Bioengineering, University of California, San Diego, CA 92093-0412, USA.
Diagnostics (Basel). 2021 May 27;11(6):971. doi: 10.3390/diagnostics11060971.
The red blood cell has become implicated in the progression of a range of diseases; mechanisms by which red cells are involved appear to include the transport of inflammatory species via red cell-derived vesicles. We review this role of RBCs in diseases such as diabetes mellitus, sickle cell anemia, polycythemia vera, central retinal vein occlusion, Gaucher disease, atherosclerosis, and myeloproliferative neoplasms. We propose a possibly unifying, and novel, paradigm for the inducement of RBC vesiculation during vascular flow of red cells adhered to the vascular endothelium as well as to the red pulp of the spleen. Indeed, we review the evidence for this hypothesis that links physiological conditions favoring both vesiculation and enhanced RBC adhesion and demonstrate the veracity of this hypothesis by way of a specific example occurring in splenic flow which we argue has various renderings in a wide range of vascular flows, in particular microvascular flows. We provide a mechanistic basis for membrane loss and the formation of lysed red blood cells in the spleen that may mediate their turnover. Our detailed explanation for this example also makes clear what features of red cell are involved in the vesiculation process and hence require quantification and a new form of quantitative indexing.
红细胞已被认为与一系列疾病的进展有关；红细胞参与疾病的机制似乎包括通过红细胞衍生的囊泡运输炎症物质。我们综述了红细胞在糖尿病、镰状细胞贫血、真性红细胞增多症、视网膜中央静脉阻塞、戈谢病、动脉粥样硬化和骨髓增殖性肿瘤等疾病中的作用。我们提出了一种可能统一且新颖的范式，用于解释在附着于血管内皮以及脾红髓的红细胞的血管流动过程中红细胞囊泡化的诱导机制。事实上，我们综述了支持这一假说的证据，该假说将有利于囊泡化以及增强红细胞黏附的生理条件联系起来，并通过脾血流中发生的一个具体例子证明了这一假说的真实性，我们认为这个例子在广泛的血管流动中，特别是微血管流动中具有多种表现形式。我们为脾脏中膜的丢失和裂解红细胞的形成提供了一个机制基础，这可能介导了它们的更新。我们对这个例子的详细解释也明确了红细胞的哪些特征参与了囊泡化过程，因此需要进行量化以及一种新的定量索引形式。
