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Mitochondrial p53 is apparently linked to intrinsic apoptosis signaling, so this relocalization is posited to increase susceptibility to apoptosis specifically in senescent cells

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Our data show that suppressing production of NADPH leaves the ER more oxidizing (or, to be more precise, more resistant to reduction) and, consequently, more resistant to an exogenous ER stressor (Gansemer et al., 2020)

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In the same year, a related report in the International Journal of Obesity described fat-oxidation and body-weight-associated changes in obese mice from chronic treatment with a modified C-terminal hGH fragment, notably without inducing hyperglycemia or reducing insulin secretion [6]