In a global context of advanced aging, geriatric diseases such as frailty syndrome face challenges in the search for biomarkers and preventive strategies. Frailty has been associated with atherothrombotic pathologies. Circulating microvesicles (cMVs), phospholipid‐rich vesicles with a size of 0.1–1.0 μm, have been shown to participate in atherothrombosis onset and progression. We have hypothesized that cMVs from platelets, and vascular and immune cells, are increased in frail older adults. To verify this, a prevalent‐case control study was designed with 28 frail older and 27 nonfrail older adults older than 64 years. Frailty was defined by Fried's phenotype. Total cMVs, annexin V positive (AV+)‐cMVs, and annexin V negative (AV⁻)‐cMVs derived from blood and vascular cells were measured by flow cytometry. In the analysis of total cMVs, the frail group presented higher levels of CD14⁺/CD142⁺ (p = .042), CD41a⁺/CD142⁺ (p = .041), and CD56⁺ (p = .025), CD14⁺cMVs (p = .043), and CD16⁺/CD14⁺ (p = .019) cMVs levels. Within the phosphatidylserine‐exposing cMVs (AV⁺), the frail group showed higher CD14⁺/AV⁺ (p = .044), CD9⁺/AV⁺ (p = .031), P2RY12⁺/AV⁺ (p = .028), and CD235a⁺/AV⁺ (p = .043) cMVs concentrations. Finally, within AV⁻ cMVs, the frail group showed higher CD142⁺/CD41a⁺/AV⁻ cMVs concentrations originated from platelets (p = .027), CD56⁺/AV⁻ originated from natural killer cells (p = .022), and CD34⁺/AV⁻ cMVs from hematopoietic stem cells (p = .037). In summary, frail older adults present higher concentrations of platelet‐, leukocyte‐, and hematopoietic cell‐derived cMVs compared to robust age‐matched older adults. These cMVs may be involved in the deregulation of the immune system, endothelial damage, and increased risk of thrombosis associated with frailty.

中文翻译：

---

虚弱的老年人显示出明显的血浆微泡特征，表明具有促血栓形成和促炎表型。

在全球老龄化背景下，衰弱综合征等老年疾病在寻找生物标志物和预防策略方面面临挑战。虚弱与动脉粥样硬化血栓形成病理有关。循环微泡 (cMV) 是一种大小为 0.1-1.0 μm 的富含磷脂的囊泡，已被证明参与动脉粥样硬化血栓形成的发生和进展。我们假设来自血小板、血管和免疫细胞的 cMV 在体弱的老年人中增加。为了验证这一点，设计了一项流行病例对照研究，其中包括 28 名体弱的老年人和 27 名 64 岁以上的非体弱老年人。虚弱是由弗里德的表型定义的。总 cMV、膜联蛋白 V 阳性 (AV+)-cMV 和膜联蛋白 V 阴性 (AV ^-)-来自血液和血管细胞的 cMV 通过流式细胞术测量。在总 cMV 的分析中，体弱组表现出更高水平的 CD14 ⁺ /CD142 ⁺ ( p  = .042)、CD41a ⁺ /CD142 ⁺ ( p  = .041) 和 CD56 ⁺ ( p  = .025)、CD14 ⁺ cMV ( p  = .043) 和 CD16 ⁺ /CD14 ⁺ ( p  = .019) cMV 水平。在暴露于磷脂酰丝氨酸的 cMV (AV ⁺ ) 中，体弱组表现出更高的 CD14 ⁺ /AV ⁺ ( p  = .044)、CD9⁺ /AV ⁺ ( p  = .031)、P2RY12 ⁺ /AV ⁺ ( p  = .028) 和 CD235a ⁺ /AV ⁺ ( p  = .043) cMVs 浓度。最后，在 AV ^- cMVs 中，虚弱组表现出更高的 CD142 ⁺ /CD41a ⁺ /AV ^- cMVs 浓度源自血小板 ( p  = .027)，CD56 ⁺ /AV ^-源自自然杀伤细胞 ( p  = .022)，以及CD34 ⁺ /AV ^-来自造血干细胞的 cMV ( p = .037）。总之，与健壮的年龄匹配的老年人相比，体弱的老年人表现出更高浓度的血小板、白细胞和造血细胞来源的 cMV。这些 cMV 可能与免疫系统失调、内皮损伤和与虚弱相关的血栓形成风险增加有关。