KLF2-dependent transcriptional regulation safeguards the heart against pathological hypertrophy

Our previous single-cell RNA sequencing study in the adult human heart revealed that cardiomyocytes from both the atrium and ventricle display high activities of KLF2 regulons. However, the role of the transcription factor KLF2 in cardiomyocyte biology remains largely unexplored. This study provides the first evidence that transcription factor KLF2 serves as a negative regulator of cardiac hypertrophy. Our findings highlight the therapeutic potential of enhancing KLF2 expression, particularly through simvastatin administration, as a promising strategy in the treatment of cardiac hypertrophy.