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. 2021 Aug 19;9:668377. doi: 10.3389/fcell.2021.668377

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Copyright © 2021 Wang, Wang, Zhang, Wu, Shi and Yuan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ALKBH5 can suppress HASMC proliferation, promote HAEC apoptosis, and facilitate AD progression in AngII-infused mice. (A,B) Both CCK8 and EdU assays found that overexpression of ALKBH5 significantly inhibited HASMC proliferation while knockdown of ALKBH5 led to increased HASMC proliferation. (C) Flow cytometry analysis showed that ALKBH5 overexpression notably promoted HAEC apoptosis while its knockdown significantly suppressed HAEC apoptosis. (D) The interference effects on ALKBH5 expression in AngII-infused C57BL/6J mice were examined. (E) KIAA1429 overexpression reduced the incidence while its knockdown increased the incidence of AD in AngII-infused mice. (F) Mice in the sh-ALKBH5 group and LV-ALKBH5 group had longer and shorter survival times compared to the control group, respectively. Data are presented as the mean ± SEM (N ≥ 3 per group); *p < 0.05.