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Sustained cardiac function depends on circadian REV-ERBs. Here, Dierickx et al. show that circadian nuclear receptors REV-ERBα and β are indispensable to establish the transcriptional program that controls cardiac metabolism and NAD+ production. Deregulation of REV-ERBs leads to dilated cardiomyopathy and premature death.
Sick heart and vessels skew hematopoiesis toward inflammatory myeloid cells. Rhode et al. show that hypertension, atherosclerosis and myocardial infarction cause endothelial dysfunction in bone marrow (BM), which in return causes overproduction of inflammatory myeloid cells and systemic leukocytosis in mice. This process is mediated by VEGF signaling, IL-6 and versican production by the BM endothelium.
