Why the study?
Cardiac hypertrophy is a key process in remodeling and heart failure progression, but the specific regulatory involvement of microRNAs remains incompletely understood.
Population
Preclinical model of Angiotensin II (Ang II)-induced cardiac hypertrophy
Comparison
Modulation of miR-300-3p and ACOX1 expression vs Control models
Design
Preclinical
Key result
DNMT1-regulated promoter hypomethylation enhances miR-300-3p expression, which suppresses ACOX1 and promotes ferroptosis in Ang II-induced cardiac hypertrophy.
Authors
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Should not change hypertrophy management; hypothesis-generating for miR-300-3p/ACOX1/GPX4 targeting in remodeling.
The study identifies the miR-300-3p/ACOX1/GPX4 axis as a novel regulatory pathway in cardiac hypertrophy and ferroptosis, offering potential new therapeutic targets.
Li et al. (2026) studied Cardiac hypertrophy. miR-300-3p was evaluated on Ang II-induced cardiac hypertrophy and ferroptosis. DNMT1-regulated promoter hypomethylation enhances miR-300-3p expression, which suppresses ACOX1 and promotes ferroptosis in Ang II-induced cardiac hypertrophy.