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Well established mechanisms include myocardial energy depletion due to impaired adenosine triphosphate (ATP) synthesis and mitochondrial uncoupling, and increased mitochondrial oxidative stress

30, 31, 32, 33 Interestingly, experimental data also suggest that an increased production of H 2 O 2 can represent a critical component of the neuroprotective processes that occur during or after ischemic stroke

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Moreover, dendritic spines that receive most excitatory synaptic inputs have been shown to contain no mitochondria (Kasthuri et al., 2015), despite being sites of intense energy utilization

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The eumelanin within melanosomes shields cells from further UVR damage by absorbing, reflecting and refracting light