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Many pharmaceutical companies have tried to develop drugs that target Mcl-1, but this has been difficult because the interaction between Mcl-1 and its target protein occurs in a long stretch of 20 to 25 amino acids, which is difficult to block with the small molecules typically used as drugs

Chronic hyperglycemia-induced ROS overproduction, primarily derived from mitochondrial ETC leakage and NOX activation, leads to eNOS uncoupling due to BH4 oxidation, reducing NO bioavailability and impairing vasodilation (Kowluru and Mishra, 2017), while in diabetic nephropathy, podocyte injury results from NOX4-derived O 2 and mitochondrial ROS-mediated apoptosis (Jha et al., 2024)

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In addition, our understanding of the iron cycling imbalance and ferroptosis in the pathological context of bone and joint diseases is lacking

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