Figure 7.

Effect of aging, NLPR3 inflammasome, and melatonin therapy on the cardiac circadian system. Aging produced minor changes in the Clock acrophase, loss of rhythmicity in Per2 and Rorα, and a tendency towards dampening the mesor. NLRP3 inflammasome modified the acrophase of Clock, Per2, and Rorα. Expression of Rev-erbα was not influenced by mouse genotype. Melatonin re-established the acrophase and rhythm of these three genes. Morphological analysis revealed age-associated impairments in cardiac muscle fibers, which were less harmful in NLRP3-knockout mice. Melatonin treatment preserved the structure of cardiomyocytes in all experimental groups.