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Critical for bone healing, less relevant for avascular cartilage but important for subchondral bone supporting cartilage
In a healthy body, this system operates in a state of delicate homeostasiscapable of mounting a fierce defense against invading pathogens while simultaneously knowing exactly when to stand down to prevent collateral tissue damage
Many cardiovascular risk factors such as diabetes mellitus, hypertension and hyperlipidemia are demonstrated to stimulate the interaction of Cav-1 and eNOS, reduce nitric oxide production resulting in endothelial dysfunction and subsequently the formation of atherosclerotic lesion 41,42,43
Consistently, SOD1 G93A transgenic mice exhibited ferroptotic features and neurotoxic glial activation resembling those observed in ALS patient spinal cords and in vitro models
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