Targeting the undruggable transcription factor, KLF5, with a peptidomimetic small molecule, NC114, attenuates pressure overload-induced cardiac remodeling and fibrosis.
利用肽模拟小分子 NC114 靶向不可成药的转录因子 KLF5，可减轻压力超负荷引起的心脏重塑和纤维化。
期刊:Scientific Reports
影响因子:3.9
doi:10.1038/s41598-025-32155-y
Methatham Thanachai, Kimura Natsuka, Tomida Shota, Ishima Tamaki, Taguchi Yuki, Uosaki Hideki, Sakashita Eiji, Endo Hitoshi, Nagai Ryozo, Aizawa Kenichi
