Key result
SOX4 knockdown reduces murine cardiac hypertrophy by modulating SIRT3 transcription and oxidative stress.
Why the study?
Pathological cardiac hypertrophy can lead to heart failure, but the role of the transcription factor SOX4 in pathological cardiac hypertrophy remains unclear.
Does knocking down SOX4 expression reduce the hypertrophic response in Ang II-treated NRCMs and mouse hearts?
Does knocking down SOX4 expression reduce the hypertrophic response in Ang II-treated NRCMs and mouse hearts?
SOX4 promotes pathological cardiac hypertrophy by inhibiting SIRT3 and increasing oxidative stress, suggesting its knockdown as a potential therapeutic target.
SOX4 knockdown attenuates hypertrophy in rodent models; leaves open therapeutic translation to human HF.
Pathological cardiac hypertrophy can lead to heart failure, making its prevention crucial. SOX4, a SOX transcription factor, regulates tissue growth and development, although its role in pathological cardiac hypertrophy is unclear. We found that the SOX4 expression was elevated in hypertrophic hearts and angiotensin II (Ang II)-treated neonatal rat cardiomyocytes (NRCMs), and knocking down the SOX4 expression in NRCMs and mouse hearts significantly reduced the hypertrophic response. Mechanistically, SOX4 can bind to the SIRT3 promoter, inhibit SIRT3 transcription and expression, and thus affect downstream MnSOD acetylation levels, leading to abnormal increases in ROS and oxidative stress levels and promoting the occurrence of cardiac hypertrophy. In conclusion, this study identified a new role for SOX4 in regulating cardiac hypertrophy, and decreasing SOX4 expression may be a potential treatment for pathological cardiac hypertrophy.
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Shen et al. (2023) studied Pathological cardiac hypertrophy. SOX4 knockdown was evaluated on Hypertrophic response.
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