Sun SY, Zhang GH, Lv SM, et al
Soma N, Uchida Y, Kouyama JI, et al
Physicochemical properties of CSDs To further investigate the lability of the CSDs of interest we calculated the torsional energies of the disulfide bonds
Moreover, acquired gliotoxin resistance in A
The difference likely reflects underlying metabolic differences, concurrent medications, and disease severity rather than any differential drug effect

rather, the dominant effect is mediated through altered carnitine availability ( Cytoprotective, vascular, and mitochondrial effects Meldonium has been reported to exert vasodilatory effects, likely via nitric-oxiderelated pathways, with potential implications for blood flow and oxygen delivery during exertion ( Hypoxia and intense exercise promote inflammatory activation and oxidative stress that contribute to mitochondrial dysfunction, often via disturbed fusionfission balance and accumulation of damaged mitochondria/mtDNA ( Mitochondrial remodeling in response to Meldonium is not necessarily benign: increased mitochondrial turnover or exercise-induced stress can elevate ROS and mtDNA vulnerability, particularly with impaired antioxidant defenses or DNA repair ( In athletes, prolonged high-intensity exertion may lead to athletic heart syndrome, characterized by cardiac hypertrophy, inflammation, oxidative stress, mitochondrial dysfunction, and accumulation of acylcarnitines with disturbed substrate oxidation ( -oxidation and activating glucose-metabolic pathways (e.g., 6-phosphofructokinase and pyruvate dehydrogenase), Meldonium shifts ATP production from lipids toward carbohydrates during exercise, which may reduce oxidative stress and improve metabolic flexibility ( Preclinical performance data are mixed
