{Reference Type}: Journal Article
{Title}: Ischemia-reperfusion injury in human AC16 cardiomyocytes is modulated by AXIN1 depending on c-Myc regulation.
{Author}: Li J;Wang H;Chen L;Zhong J;Wang J;Xiao J;
{Journal}: Ann Med Surg (Lond)
{Volume}: 85
{Issue}: 10
{Year}: 2023 Oct
暂无{DOI}: 10.1097/MS9.0000000000001139
{Abstract}: <B>UNASSIGNED: </B>A major consequence of acute myocardial infarction is myocardial ischemia-reperfusion (I/R) injury. Collecting proof demonstrates that AXIN1 assume a basic part in different disease; however, the role of AXIN1 in I/R injury remains to a great extent obscure.<BR><B>UNASSIGNED: </B>The I/R injury model on AC16 cells was constructed. siRNA transfection was used to knockdown AXIN1. The qRT-PCR assays and western blot assays were used to detect the expression level of AXIN1 and other key proteins. CCK-8 assays and cell apoptosis assays were used to detect cell proliferation and cell apoptosis.<BR><B>UNASSIGNED: </B>AXIN1 was significantly overexpressed in an in vitro model of I/R injury. Knockdown of AXIN1 significantly restored the cell proliferation inhibition caused by IR injury, while inhibiting apoptosis and inflammation. Further mechanistic studies revealed that the transcription factor c-Myc could regulate the expression of AXIN1. The effects of I/R injury on AC16 cells after overexpression of c-Myc were reversed by knockdown of AXIN1. Meanwhile, AXIN1 could regulate the SIRT1/p53/Nrf 2 pathway.<BR><B>UNASSIGNED: </B>Our results show an important role for AXIN1 and provide new targets for avoiding and treating I/R injury.