['Endothelial microparticles (EMPs) are small vesicular structures that serve as a marker of endothelial function. Angiotensin II receptor type 1 autoantibody (AT1-AA) can cause endothelial dysfunction. However, whether AT1-AA promotes EMPs formation and the mechanism remains obscure.', "The titres of sera AT1-AA of 126 hypertensive patients and 30 normotensive individuals were evaluated by ELISA. EMPs in the sera and the supernatants of human umbilical vein endothelial cells (HUVECs) were measured by flow cytometry. The phosphorylation levels of mitogen-activated protein kinase (MAPK) pathways in HUVECs treated by AT1-AA were assessed and their correlation with microparticle formation was also analysed. Furthermore, the production of intracellular reactive oxygen species (ROS) and nitric oxide in HUVECs was examined after incubation with 'injured' endothelial microparticle (iEMPs) (EMPs derived from AT1-AA treated HUVECs).", "The positive rate of AT1-AA in 126 hypertensive patients was 21.4% (27/126), and higher than that in normotensive individuals [3.3% (1/30), P\u200a<\u200a0.01]. Circulating EMP (CD31+/CD42b-) levels were corresponding to the AT1-AA titres in hypertensive group (r(2)\u200a=\u200a0.3661, P\u200a<\u200a0.01). AT1-AA promoted EMPs generation from HUVECs in a time and dose-dependent manner than the vehicle or nonspecific IgG. Meanwhile, AT1-AA significantly elevated phosphorylation level of P38 and ERK in HUVECs. Lorsartan and P38 inhibitor could suppress the AT1-AA's stimulation effect on EMPs generation. Moreover, the iEMP greatly increased ROS production and reduced nitric oxide synthesis in HUVECs."] Do angiotensin II receptor type 1 autoantibodies promote endothelial microparticles formation through activating p38 MAPK pathway?