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In addition, a one-size-fits-all approach may not be suitable for OA due to the confusing heterogeneity of the disease

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Chronic mitochondrial ROS production in HF further drives myocyte apoptosis via ROS-mediated activation of caspases and mPTP opening, fibrosis through ROS-activated TGF- signaling in fibroblasts, and electrical instability due to oxidative damage to ion channels, increasing arrhythmia risk