What question did this study set out to answer?

The research aims to investigate the effects of the small molecule NC114 on KLF5-related cardiac remodeling and fibrosis during pressure overload-induced heart failure.

January 15, 2026Scientific ReportsOpen Access

Targeting the undruggable transcription factor, KLF5, with a peptidomimetic small molecule, NC114, attenuates pressure overload-induced cardiac remodeling and fibrosis

View Full Paper

Ask AI

Bookmark

Authors

TMThanachai MethathamJichi Medical University NKNatsuka KimuraJichi Medical University STShota TomidaJichi Medical University

Discussion

Member takes

Implication

Administration of NC114 improves cardiac function and reduces fibrosis in mice with pressure overload-induced heart failure, suggesting a novel therapeutic approach.

Key Points

The research aims to investigate the effects of the small molecule NC114 on KLF5-related cardiac remodeling and fibrosis during pressure overload-induced heart failure.
Utilized adult C57BL/6J male mice undergoing transverse aortic constriction (TAC) or sham surgery.
Administered NC114 or vehicle post-surgery to evaluate cardioprotective effects.
Conducted gene expression analysis for Klf5 and related markers.
Performed metabolomic profiling to assess metabolic changes post-treatment.
NC114-treated mice showed preserved cardiac function and reduced heart weight-to-body weight ratio.
Observed a marked reduction in interstitial fibrosis in TAC mice treated with NC114.
Gene expression analysis indicated decreased expression of Klf5, Nppb, Tgfb1, PAI-1, Col1a1, and Fn1.
NC114 suppressed oxidative stress and decreased phosphorylation of PKCδ and expression of HIF-1α.

Cite This Study

Methatham et al. (2026) studied this question.

synapsesocial.com/papers/69683e135818e7dbd7c630fa https://doi.org/10.1038/s41598-025-32155-y

View Full Paper

Ask AI

Bookmark

Implication

Administration of NC114 improves cardiac function and reduces fibrosis in mice with pressure overload-induced heart failure, suggesting a novel therapeutic approach.

Targeting the undruggable transcription factor, KLF5, with a peptidomimetic small molecule, NC114, attenuates pressure overload-induced cardiac remodeling and fibrosis

Discussion

Member takes

Implication

Key Points

Cite This Study

Targeting the undruggable transcription factor, KLF5, with a peptidomimetic small molecule, NC114, attenuates pressure overload-induced cardiac remodeling and fibrosis

Discussion

Member takes

Implication

Key Points

Cite This Study

Also Consider

Also Consider