Key result
Post-MI transcriptomic profiling reveals 9 gene clusters driving phase-specific immune, fibrotic, and metabolic shifts.
Why the study?
Prior studies characterized transcriptional programs in post-infarct remodeling at discrete timepoints, leaving a need for a temporal map of gene expression changes from minutes to weeks post-myocardial infarction.
May guide timed interventions in post-MI remodeling; extends prior discrete timepoint studies with continuous phase mapping.
Myocardial infarction (MI) initiates a cascade of biological changes ending in cardiac remodeling and heart failure. Recent studies have characterized transcriptional programs in post-infarct remodeling, focusing on discrete timepoints. This study adopted a complementary approach by constructing a temporal map of gene expression changes from minutes to weeks post-myocardial infarction. Two mouse RNA-sequencing datasets were integrated, covering post-infarction timepoints from 10 min to 28 days. Expression data were analyzed using clustering, functional enrichment, and network-based hub gene analysis to define distinct gene expression modules. Nine clusters were identified, including immune activation, extracellular matrix remodeling, mitochondrial dysfunction, and circadian rhythm disruption. Immune signatures peaked between 1 and 72 h post-MI, fibrotic remodeling and cell proliferation dominated the 3-7-day window, and fibrosis still extended to the 28-day mark. Mitochondrial dysfunction persisted into the 28th day, along with circadian rhythm and metabolic dysfunction. These trajectories highlight distinct pathways and the potential therapeutic windows across infarction. This research offers a timeline for temporally guided therapies in MI. Identifying distinct pathways and hub genes to provide a molecular basis for future studies targeting inflammation, fibrosis, metabolism, and chronobiology. These results may accelerate the development of more effective treatments for myocardial infarction.
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Ardo Sanjaya (2025) studied Myocardial infarction. Myocardial infarction (LAD ligation) vs. Sham controls was evaluated on Temporal gene expression changes and distinct gene expression modules. Time-series transcriptomic analysis of mouse hearts post-myocardial infarction identified nine distinct gene expression clusters, revealing phase-specific transitions from early immune activation to late fibrotic and metabolic remodeling.
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