Key result
Metabolic stress activates immune cells to drive low-grade inflammation in cardiometabolic HFpEF.
Why the study?
Low-grade inflammation is triggered by metabolic imbalances in cardiometabolic heart failure, with immune cells causally implicated in experimental metabolic syndromes.
This review discusses evidence for the contribution of metabolic stress to immune cell activation during cardiometabolic heart failure with preserved ejection fraction and related therapeutic approaches.
No immediate change to HFpEF care; leaves open whether targeting metabolic-immune pathways improves outcomes.
Inflammation is triggered by imbalances to systemic and cellular metabolism. This occurs in the setting of cardiometabolic heart failure, for which low‐grade inflammation is a commonly reported feature. In experimental models, immune cells are causal determinants in the pathophysiology of metabolic syndromes. Herein we discuss evidence for the contribution of metabolic stress to immune cell activation during cardiometabolic heart failure with preserved ejection fraction. We also discuss related therapeutic approaches along the way.
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Pereira et al. (2026) studied this question. Metabolic stress activates immune cells in cardiometabolic heart failure with preserved ejection fraction, contributing to low-grade inflammation.
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