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Davis, N

It is widely known that mitochondrial dysfunction (high ROS production, apoptotic cells, decreased m, and low cellular ATP levels) boosts the pathogenesis of KOA because it involves lipid homeostasis and cytokine release and promotes cell apoptosis [14, 15]

The basis for use of beta-adrenergic blocking agents (beta blockers) is that excessive thyroid hormone mimics many of the effects of excess adrenalin
doi: 10.1007/s00213-007-0840-x