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Cardiomyocytes apoptosis reperfusion injury - Wiley Online Library

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Last Updated: 23 January 2022

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Downregulation of tripartite motif protein 11 attenuates cardiomyocyte apoptosis after ischemia/reperfusion injury via DUSP1‐JNK1/2

Consequently, this research was intended to investigate the effects of tripartite motif protein 11 on cardiomyocytes I/R injury and the underlying mechanism. Following the detection of oxidative stress-related pathways by TRIM11 downregulation in I/R cells, cell proliferation, and apoptosis at 48 h, as well as the associated molecular changes in oxidative stress-related pathways, oxidative stress responses were reported. In addition, the overexpression of TRIM11 in AC16 cells led to apoptosis in AC16 cells, and JNK1/2 inhibition and DUSP1 overexpression potently countered the initiation of TRIM11 overexpression in AC16 cells. The downregulation of TRIM11 reduces apoptosis in AC16 cells after I/R injuries, most likely through the DUSP1-JNK1/2 pathways, according to these.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/cbin.11716

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions