Key result
STAT3 expression is reduced in cardiac pericytes in HFpEF, and its loss induces cellular senescence and impairs pericyte adhesion, contributing to pericyte loss.
Why the study?
Heart failure with preserved ejection fraction is characterised by reduced pericyte coverage, but the role of pericytes remains less understood compared to other cardiac cell types.
Reduced STAT3 expression is a hallmark of cardiac pericytes in HFpEF, and its loss drives pericyte senescence and impaired adhesion, highlighting a potential mechanism for microvascular dysfunction in HFpEF.
STAT3 loss may drive pericyte senescence in HFpEF; animal data leave open whether targeting it alters disease progression in patients.
Heart failure with preserved ejection fraction (HFpEF) accounts for half of heart failure cases and is characterised by reduced pericyte coverage. While the contributions of other cardiac cell types to HFpEF are well-studied, the role of pericytes remains less understood. Using murine single-nucleus RNA sequencing to study cardiac pericytes in HFpEF, we identified reduced STAT3 expression as a hallmark of HFpEF pericytes. Mechanistic studies in vitro revealed that STAT3 deletion induces cellular senescence and impairs pericyte adhesion, recapitulating HFpEF-like characteristics. These findings suggest that STAT3 is crucial for maintaining pericyte homeostasis and highlight its reduction as a potential driver of pericyte loss, a defining feature of HFpEF.
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Vanicek et al. (2025) studied Heart failure with preserved ejection fraction (HFpEF). STAT3 knockdown vs. Control siRNA was evaluated on Cellular senescence and pericyte adhesion. STAT3 expression is reduced in cardiac pericytes in HFpEF, and its loss induces cellular senescence and impairs pericyte adhesion, contributing to pericyte loss.
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