Why the study?
Matrix remodeling outcomes largely dictate post-MI survival, and human-restricted noncoding regulatory elements worsen fibrosis, but their mechanism of action remains elusive.
Population
Induced pluripotent stem cell-derived cardiac fibroblasts
Comparison
Inflammatory ligand activation vs AP-1 pathway inhibition and 9p21 noncoding polymorphisms
Design
In vitro preclinical mechanistic study
Authors
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Does not support AP-1 targeting post-MI; hypothesis-generating for human fibroblast fibrosis mechanisms.
AP-1 signaling is a critical modulator of fibrotic stress responses in cardiac fibroblasts, which can be influenced by noncoding regulatory elements such as the 9p21 locus.
Whitehead et al. (2023) studied this question.
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