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Under stress, neurotrophic factors released from the myocardium trigger sympathetic nerve sprouting and hyperinnervation in the atria, thereby forming a structural “neural substrate” conducive to AF

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Treatment of fibroblasts from COPD patients with hemin to activate HO-1 results in reduced cellular senescence, improved mitochondrial function, and reduced ROS production [122] Since Nrf2 activates many other antioxidant genes in addition to HO-1, this suggests that activators of Nrf2 and inhibitors of Keap1 might be even more effective against oxidative stress in COPD