Inhibiting STAT5 significantly attenuated Ang II-induced cardiac dysfunction and inflammation

by Selleckchem | Oct 28 2023

Cardiac hypertrophy is a compensatory response to chronic pressure overload. Excessive angiotensin II is an important inducer of cardiac hypertrophy. Signal transducers and activators of transcription 5(STAT5), a member of STATs family which can mediate the transcription of interferon (IFN) genes and immune response has recently been reported to have a close link with non-tumor diseases. However, much remains unknown about how STAT5 might be involved in the progression of hypertrophy. Herein, STAT5-IN-1, a STAT5 inhibitor, was orally administered to Ang II-induced mice. Ang II-stimulated H9c2s cells were used as cell models for the in vitro experiment. Efforts were made to investigate the effects of STAT5-IN-1 in Ang II-induced mice, along with potential mechanism that might account for these effects, which involved treatment with STAT5 inhibitor and the use of siRNA-induced gene silencing. The findings demonstrated that STAT5 inhibitor resulted in a substantial decrease in cardiac hypertrophy in Ang II-induced mice and that this effect is mediated by decreasing inflammation, thus identifying one mechanism of Ang II-induced STAT5 activation. Based on these findings, it can be argued that targeting STAT5 mighted be considered as a potential therapeutic strategy for reducing hypertrophy.

Comments:

The paragraph you provided describes a study that aimed to investigate the role of STAT5, a member of the Signal Transducers and Activators of Transcription (STAT) family, in cardiac hypertrophy induced by excessive angiotensin II (Ang II). Cardiac hypertrophy refers to an enlargement of the heart muscle cells in response to chronic pressure overload. The researchers used an inhibitor called STAT5-IN-1 to block the activity of STAT5 and examined its effects in both in vivo and in vitro experiments.

In the study, Ang II-induced mice were orally administered with the STAT5 inhibitor, and H9c2s cells (a cell line commonly used to study cardiac cells) were stimulated with Ang II to mimic the in vitro conditions. The researchers wanted to observe the effects of inhibiting STAT5 on cardiac hypertrophy and investigate the potential mechanisms underlying these effects. They also utilized siRNA-induced gene silencing to further understand the role of specific genes in the process.

The findings of the study demonstrated that inhibiting STAT5 with the STAT5-IN-1 inhibitor resulted in a significant decrease in cardiac hypertrophy in the Ang II-induced mice. The researchers also identified that this effect was mediated by reducing inflammation, providing insights into one mechanism of Ang II-induced STAT5 activation. Therefore, the study suggests that targeting STAT5 may have therapeutic potential in reducing hypertrophy.

It is important to note that this paragraph represents a hypothetical summary of a research study and the findings mentioned are not based on real experimental results. The paragraph is constructed based on the information provided in your question and may not accurately represent the actual findings or conclusions of any specific study.