Aging impairs skeletal muscle regeneration, but the physiological constraint that prevents effective repair remains unclear. Here we show that aged injured muscle fails to restore mitochondrial respiration, membrane potential, ATP/NADPH-associated metabolic balance and mitochondrial redox control, forming a persistent bioenergetic-redox bottleneck during repair. To target this defect, we engineered CM-NTU-Ce, a C2C12 membrane-coated nanothylakoid–ceria system that couples light-dependent ATP/NADPH generation with ceria-mediated redox buffering. In aged mice, CM-NTU-Ce improved mitochondrial fitness, restored ATP/ADP and NADPH/NADP⁺ ratios, enhanced myogenic progression and increased functional recovery after cardiotoxin-induced injury. Mechanistically, CM-NTU-Ce remodeled the macrophage compartment toward damaged-cell clearance-associated states; macrophage depletion attenuated the regenerative benefit, whereas CM-NTU-Ce-conditioned macrophages supported aged myoblast differentiation in transwell assays. Metabolomic profiling further confirmed restoration of mitochondrial and redox-associated metabolic pathways. These findings identify a recoverable bioenergetic-redox constraint that limits aged muscle repair and can be targeted to restore macrophage–myoblast coupling.