Brain heart interfaces: The neurovascular unit in the aging heart

In the modern society, increased life expectancy has led to a shift in the distribution of relevant diseases. Hence, age-related pathologies, particularly cardiovascular diseases, rank as leading causes of death globally1. During aging, the heart undergoes various structural and cellular changes that underlie cellular alterations and result in reduced cardiac function2,3. The cardiac autonomic nervous system has caught special attention in this context as a decline of sympathetic fibers in the aging left ventricle was associated with decreased heart rate variability (HRV) and increased arrhythmic risk. As putative mechanism nervous regression was suggested as a consequence of a disturbed neurovascular interaction possibly driven by vascular senescence. Since heart failure with preserved ejection fraction (HFpEF) is a prominent age-related cardiovascular disease, the present proposal is meant to understand the involvement of the neurovascular unit in the pathophysiology of HFpEF.