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Metabolic Stress and Immune Activation in Heart Failure With a Preserved Ejection Fraction
Ana Pereira1, Santiago Alvarez-Argote1, Isaac Meite1
1Department of Pathology, Feinberg School of Medicine and Center for Cardiovascular Innovation at the Heart Center, Northwestern University & Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois, USA.
Immunological Reviews
|January 13, 2026
Summary
Metabolic stress drives inflammation in cardiometabolic heart failure. This review explores how metabolic imbalances activate immune cells, contributing to heart failure with preserved ejection fraction and potential therapies.
Area of Science:
- Cardiology
- Immunology
- Metabolic Disorders
Background:
- Inflammation is a key feature of cardiometabolic heart failure.
- Immune cells play a critical role in metabolic syndrome pathophysiology.
- Metabolic stress disrupts systemic and cellular balance, triggering inflammation.
Purpose of the Study:
- To examine the role of metabolic stress in immune cell activation.
- To understand the contribution of metabolic stress to heart failure with preserved ejection fraction.
- To discuss potential therapeutic strategies targeting metabolic pathways.
Main Methods:
- Review of experimental models and existing literature.
- Analysis of the link between metabolic stress and immune cell function.
- Exploration of therapeutic targets in cardiometabolic heart failure.
Main Results:
- Metabolic stress directly contributes to immune cell activation in heart failure.
- Imbalances in metabolism are central to the inflammatory processes observed.
- Evidence supports immune cells as determinants in metabolic syndrome progression.
Conclusions:
- Metabolic stress is a significant driver of inflammation in cardiometabolic heart failure.
- Targeting metabolic pathways may offer novel therapeutic avenues.
- Further research into immune cell-metabolism interactions is warranted.
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