Summary
This systems genetics study, conducted across diverse inbred mouse strains, identified coagulation factor XI (FXI)—a liver-derived protein—as a protective factor against diastolic dysfunction and heart failure with preserved ejection fraction. The protective mechanism operates independently of FXI's canonical role in coagulation; instead, FXI activates the BMP7-SMAD1/5 signalling axis in cardiac tissue, suppressing inflammatory and fibrotic gene programmes. The findings suggest a previously unrecognised tissue-tissue endocrine communication pathway linking hepatic FXI production to cardiac health.
Regional applicability
This is a mechanistic mouse model study with no direct application to UK farming or agricultural systems. The findings may have future relevance to understanding cardiovascular disease aetiology in human populations globally, but transferability depends on validation in human clinical cohorts and does not inform agricultural or soil health practice.
Key measures
Transcriptomic data, functional biomarkers of diastolic dysfunction, BMP-SMAD1/5 pathway activation, inflammation and fibrosis gene expression, FXI proteolytic activity
Outcomes reported
The study identified coagulation factor XI (FXI) as a liver-derived protein that protects against diastolic dysfunction through activation of the BMP-SMAD1/5 signalling pathway in cardiac tissue. FXI's proteolytic activity cleaves extracellular matrix-associated BMP7, thereby suppressing inflammation and fibrosis-related gene expression.
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