Abstract
Cardiovascular diseases (CVDs), including atherosclerosis, myocardial infarction and heart failure, are the leading causes of morbidity and mortality worldwide. Emerging evidence suggests a crucial role for immune cell dysfunction and inflammation in the progression of this complex set of diseases. Recent advances demonstrate that immune cells, tightly linked to CVD pathogenesis, are sensitive to environmental signals and respond by engaging immunometabolic networks that shape their behavior. Inflammatory cues and altered nutrient availability within atherosclerotic plaques or following ischemia synergize to elicit metabolic shifts in immune cells that influence the course of disease pathology. Understanding these metabolic adaptations and how they contribute to cellular dysfunction may reveal novel therapeutic approaches for the treatment of CVD. Here we provide a comprehensive summary of the metabolic reprogramming that occurs in immune cells and their progenitors during CVD, offering insights into the potential therapeutic interventions to mitigate disease progression.
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Acknowledgements
A.J.F. is supported by funding from Diabetes Australia. J.N. is supported by funding from the NHMRC (GNT202152). N.L.G. is supported by funding from the NHMRC (GNT2017335) and ARC (DP230102412). A.K. is supported by funding from the NHMRC (GNT2017420) and the Australia Research Council Discovery Grant. A.J.M. is supported by funding from the NHMRC (GNT1194329).
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A.J.F., J.N., N.L.G., A.K. and A.J.M. contributed equally to the writing and revision of the article. A.J.F. prepared the draft figures that were used as a guide for the final images.
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Fleetwood, A.J., Noonan, J., La Gruta, N. et al. Immunometabolism in atherosclerotic disorders. Nat Cardiovasc Res 3, 637–650 (2024). https://doi.org/10.1038/s44161-024-00473-5
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DOI: https://doi.org/10.1038/s44161-024-00473-5
