Key result
Myeloid NCOR1 deletion prevents diastolic dysfunction and reduces myocardial inflammation in HFpEF mice.
Why the study?
Inflammatory response is a key player in HFpEF, but the underlying mechanisms driving myocardial macrophage inflammation and pathological remodeling are poorly understood.
Does myeloid cell-specific NCOR1 deletion prevent macrophage inflammation and cardiac dysfunction in HFpEF?
Population
LV specimens from HFpEF patients and control donors, murine HFpEF models, and macrophage cell lines
Comparison
Myeloid-specific NCOR1 knockout vs control in HFpEF models and HFpEF vs controls
Design
Translational and preclinical study using human tissue, mouse models, and in vitro assays
Authors
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Supports NCOR1 as macrophage target in HFpEF; hypothesis-generating, should not yet change practice.
Does myeloid cell-specific NCOR1 deletion prevent macrophage inflammation and cardiac dysfunction in HFpEF?
NCOR1 is a key driver of macrophage inflammation in HFpEF, and its targeted deletion prevents diastolic dysfunction and exercise intolerance in preclinical models.
Gorica et al. (2025) studied Heart failure with preserved ejection fraction (HFpEF). Macrophage NCOR1 deletion vs. Control (wild-type/non-depleted) was evaluated on Diastolic dysfunction, lung congestion, exercise intolerance, and myocardial inflammation. Macrophage NCOR1 deletion in HFpEF mice prevented diastolic dysfunction, lung congestion, and exercise intolerance, and reduced myocardial inflammation.
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