Imaging Targets to Visualize the Cardiac Immune Landscape in Heart Failure

Abstract

Heart failure involves a complex interplay between diverse populations of immune cells that dynamically shift across the natural history of disease. Within this context, the character of the immune response is a key determinant of clinical outcomes. Recent technological advances in single-cell transcriptomic, spatial, and proteomic technologies have fueled an explosion of new and clinically relevant insights into distinct immune cell populations that reside within the diseased heart including potential targets for molecular imaging and therapy. In this review, we will discuss the immune cell types and their respective functions with respect to myocardial infarction remodeling, dilated cardiomyopathy, and heart failure with preserved ejection fraction. In addition, we give a brief overview regarding myocarditis and cardiac sarcoidosis as inflammatory heart failure etiologies. We will highlight markers and cell populations as targets for molecular imaging to visualize inflammation and tissue healing and discuss clinical implications including the development and implementation of precision medicine approaches.

GSTM2 alleviates heart failure by inhibiting DNA damage in cardiomyocytes

“…Consistent with their functions, mitochondrial proteins and lipid metabolism-related proteins were more abundant in healthy ventricles than in atria [ 11 ]. An increasing number of studies have reported that immune activation and inflammation are considered important drivers of cardiac remodeling and HF [ 30 , 31 ]. Interestingly, we found that the proteins that were specifically upregulated in the atria of HF samples were mainly enriched in the complement and coagulation cascades, which cause overt inflammation, thrombotic microangiopathy and end-organ damage [ 32 – 34 ]; however, the proteins that were specifically upregulated in the ventricles of HF samples were mainly enriched in the FoxO signaling pathway, which is involved in maintaining cardiomyocytes in the homeostatic state and inducing their adaptation to metabolism [ 35 , 36 ], and the apelin signaling pathway, which plays a critical role in the positive inotropic effect and maintains cardiac contractility [ 37 , 38 ].…”