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Intermittent fasting orchestrates molecular shifts, yielding cardiovascular improvements, revealing novel cardioprotective mechanisms, and suggesting innovative pharmacological strategies for cardiovascular disease prevention and treatment.

Hypoxia does not increase glycolysis in proliferating primary cells and antagonizes the increase in glycolysis caused by activation of hypoxia-inducible factor in normoxia, in part, through activation of MYC signaling pathways.

Osteoblast glucose metabolism is impaired in a mouse model for type II diabetes and can be boosted pharmacologically or genetically to alleviate diabetic osteopenia.

Mathematical analyses explore the impact of co-substrate cycling on the dynamics of cellular metabolism, and demonstrate that these dynamics can limit cellular fluxes and that co-substrate pool dynamics can be regulated to regulate fluxes.

Single-cell analysis of injured mouse sciatic nerves reveals rapid reprogramming of macrophages toward a glycolytic, proinflammatory phenotype during the early repair process.

The functional link between glycolytic flux, cell signalling and mesoderm patterning is investigated in mouse embryo.

Experimental analysis of SLC38A5 (solute carrier family 38 member 5) in mouse models and cell culture reveals its novel role as a metabolic regulator of retinal angiogenesis by controlling nutrient uptake and homeostasis in blood vessel endothelium.

An update for current knowledge gap in retinal metabolism after preterm birth and treatments for retinopathy of prematurity.

Neuronal glycolysis to restore energy consumed by ion movements is activated by engagement of the Na⁺/K⁺ pump, either directly by Na⁺ influx or indirectly, when Ca²⁺ influx is converted to Na⁺ accumulation by Na⁺/Ca²⁺ exchange.

Loss of full-length dystrophin expression causes significant molecular and functional defects in human and mouse myoblast, thus closing the vicious cycle of DMD pathology.