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This suggests the existence of mechanisms that could either delay the metabolic onset of the disease or, conversely, trigger it, and also suggests the possibility that some impairments could not be due to metabolic unbalance

In addition, studies in recent years have shown that another type of cell, the tendon stem cells (TSCs), is also present in the tendon tissue and that it has the capability to convert into tenocytes (Vigan et al., 2017)

TNF- activates the caspase-8/caspase-3/GSDME signaling axis-mediated apoptosis via complex IIb, leading to myofiber atrophy (58)

REST acts by suppressing GCLM expression, leading to decreased GCL activity and limited GSH synthesis that indicates higher sensitivity to ferroptosis