Key result
Greater coronary microvascular dysfunction in INOCA is linked to upregulation of 47 transcriptomic pathways.
Why the study?
Mechanisms underlying coronary microvascular dysfunction, a cause of ischemia with non-obstructive coronary arteries, are not well understood.
Cohort (n=28)
In female patients with INOCA, greater coronary microvascular dysfunction is associated with the upregulation of whole-blood transcriptomic pathways related to inflammation, metabolism, and cell signaling.
Answers are grounded in this paper and cite their sources.
Upregulated inflammatory and metabolic pathways may contribute to CMD in women with INOCA; hypothesis-generating and requires prospective validation before clinical translation.
BACKGROUND: Mechanisms underlying coronary microvascular dysfunction (CMD), a known cause of ischemia with non-obstructive coronary arteries (INOCA), are not well understood. METHODS: In a prospective cohort study, we investigated the whole-blood transcriptome of 28 female patients with INOCA who underwent clinically indicated invasive coronary angiography to identify pathways relevant to the pathophysiology of CMD. RESULTS: Four protein coding genes related to cell signaling and metabolism were differentially expressed and 47 transcriptomic pathways related to cell signaling, metabolism, inflammation, and sex hormone signaling were primarily upregulated with greater coronary microvascular dysfunction. CONCLUSION: Our findings support the hypothesis that inflammation leads to maladaptive microvascular remodeling and fibrosis, contributing to the pathogenesis of CMD.
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Jérôme et al. (2026) conducted a cohort in Ischemia with non-obstructive coronary arteries (INOCA) (n=28). Coronary microvascular dysfunction was evaluated on Whole-blood transcriptome (differentially expressed genes and pathways). Greater coronary microvascular dysfunction in female patients with INOCA was associated with differential expression of 4 genes and upregulation of 47 transcriptomic pathways.
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