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In the case of eNOS uncoupling due to relative intracellular BH 4 deficiency, this phenomenon could be prevented by simultaneous overexpression of the BH 4 synthesizing enzyme GTP cyclohydrolase I, which has been demonstrated in isolated cells 92 and in atherosclerotic animal models

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MIA, an inhibitor of glyceraldehyde-3-phosphate dehydrogenase, can disrupt chondrocyte glycolysis and ultimately lead to cell death, thereby contributing to cartilage degradation, subsequent alterations in subchondral bone, and the development of osteophytes 25,34