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Expression of Th-1 chemokines and chemokine receptors on the ocular surface of C57BL/6 mice: effects of desiccating stress

Jarome et al., 2013), and also results in mitochondrial swelling and damage (Maharjan et al., 2014), impaired cell differentiation, degeneration, and neuronal death via apoptosis or necrosis (Schwartz and Ciechanover, 2009

Cost-effectiveness of sodium-glucose cotransporter-2 inhibitors in the treatment of diabetic nephropathy in Japan

Oxidative stress and Parkinson: Role of astrocytes In the brain, oxidative stress and other toxic insults can trigger the overexpression and activation of neuronal nitric oxide synthase that increases NO production and may cause apoptotic cell death by inducing the release of cytochrome c from mitochondrial impairment, loss of membrane potential, the opening of permeability transition pores, and the release of proapoptotic molecules [46,47]