Key result
Cardiac USP38 knockout reduces atrial inflammation, fibrosis, and AF susceptibility post-MI in mice.
Why the study?
The role of USP38 on myocardial infarction-induced atrial inflammation, fibrosis, and associated atrial fibrillation is unclear.
Does USP38 modulation affect atrial inflammation, fibrosis, and susceptibility to atrial fibrillation after myocardial infarction in mice?
Population
USP38 cardiac conditional knockout and cardiac-specific overexpression mice with surgically constructed MI
Comparison
USP38 cardiac conditional knockout vs cardiac-specific overexpression
Design
Preclinical animal study
Follow-up
Day 7 after MI
Authors
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Findings in mice do not yet inform clinical practice; leaves open USP38 as a novel target for post-MI AF prevention.
Does USP38 modulation affect atrial inflammation, fibrosis, and susceptibility to atrial fibrillation after myocardial infarction in mice?
p-value: p=<0.05
USP38 plays a critical role in post-MI atrial inflammation and AF susceptibility via the TAK1/NF-κB pathway, highlighting a potential novel therapeutic target.
Gong et al. (2023) studied Myocardial infarction-induced atrial fibrillation. USP38 cardiac conditional knockout and overexpression vs. Sham operation and wild-type/control MI mice was evaluated on Atrial inflammation, fibrosis, and AF susceptibility (p=<0.05). USP38 cardiac-conditional knockout attenuated atrial inflammation, fibrosis, and susceptibility to atrial fibrillation after myocardial infarction in mice, whereas USP38 overexpression exacerbated them.
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