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Subsequently, it inhibited cell proliferation, promoted G0/G1 phase arrest and mitochondrial-dependent apoptosis via ERK1/2

Together, they may offer a potent combination for nutritional support for cellular and heart health

21,22,23,24 As mitochondria are responsible for energy production and cellular respiration, their dysfunction will result in muscle diseases, such as mitochondrial myopathies and myotonic dystrophy

2), which leads to a further increase in intracellular iron levels, a decrease in GSH and GPX4 activities, an increase in lipid peroxidation and a tendency to drive ferroptosis [254]