Extended Data Fig. 8: Extended analysis of human sleep restriction study and schematic of hypothesis.

a, Actigraphy measured nightly total sleep time of study participants during the habitual sleep (HS) and sleep restriction (SR) phases of the randomized crossover trial. n = 4 participants per condition. b, UMAP of scRNAseq data of PBMCs. n = 4 participants per condition. c, Pathway analysis of cluster defining genes among monocyte clusters and the top 10 cluster defining genes in cluster 2. n = 4 participants per condition. d, UMAP of chemotactic genes enriched in monocyte cluster 3. n = 4 participants per condition. e, Schematic of hypothesis. (1) Myocardial infarction activates microglia via IL-1β and (2) enhances their production of myeloid chemoattractants including CCL2 and CCL5. (3) Circulating monocytes are actively recruited to the MI brain where they release TNF which signals to glutamatergic neurons in the thalamic LPN to (4) augment sleep. (5) Enhanced sleep after MI suppresses sympathetic input to the heart which limits signalling through ADRB2 and the generation of the myeloid chemoattractants CCL3 and CCL4 to (6) suppress monocyte recruitment to the infarcted heart thus limiting inflammation and promoting healing. Data are mean ± s.e.m. Statistical analysis was done using one-way analysis of variance and two-tailed paired t-tests. *p < 0.05, **p < 0.01, ***p < 0.001.