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Immunometabolism at the Heart of Cardiovascular Disease.
DeBerge, Matthew; Chaudhary, Rajesh; Schroth, Samantha; Thorp, Edward B.
Affiliation
  • DeBerge M; Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
  • Chaudhary R; Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
  • Schroth S; Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
  • Thorp EB; Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
JACC Basic Transl Sci ; 8(7): 884-904, 2023 Jul.
Article in En | MEDLINE | ID: mdl-37547069
ABSTRACT
Immune cell function among the myocardium, now more than ever, is appreciated to regulate cardiac function and pathophysiology. This is the case for both innate immunity, which includes neutrophils, monocytes, dendritic cells, and macrophages, as well as adaptive immunity, which includes T cells and B cells. This function is fueled by cell-intrinsic shifts in metabolism, such as glycolysis and oxidative phosphorylation, as well as metabolite availability, which originates from the surrounding extracellular milieu and varies during ischemia and metabolic syndrome. Immune cell crosstalk with cardiac parenchymal cells, such as cardiomyocytes and fibroblasts, is also regulated by complex cellular metabolic circuits. Although our understanding of immunometabolism has advanced rapidly over the past decade, in part through valuable insights made in cultured cells, there remains much to learn about contributions of in vivo immunometabolism and directly within the myocardium. Insight into such fundamental cell and molecular mechanisms holds potential to inform interventions that shift the balance of immunometabolism from maladaptive to cardioprotective and potentially even regenerative. Herein, we review our current working understanding of immunometabolism, specifically in the settings of sterile ischemic cardiac injury or cardiometabolic disease, both of which contribute to the onset of heart failure. We also discuss current gaps in knowledge in this context and therapeutic implications.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: JACC Basic Transl Sci Year: 2023 Document type: Article Affiliation country: Estados Unidos

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: JACC Basic Transl Sci Year: 2023 Document type: Article Affiliation country: Estados Unidos
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