Hormonal
SIRT1 activity is context-dependent and can be inhibited by chronic oxidative stress through oxidative modifications of its cysteine residues, leading to reduced autophagy and increased inflammation.
SIRT1 is not a simple 'on/off' switch for longevity. In states of chronic stress or aging, high oxidative stress can physically inhibit SIRT1 function. Therefore, strategies to support SIRT1 must also address oxidative balance. Over-reliance on SIRT1 activators without managing overall cellular stress may be ineffective.
ROS can inhibit SIRT1 activity by evoking oxidative modifications on its cysteine residues. Decreased activity of SIRT1 enhances the NF-κB signaling, which supports inflammatory responses.
Why this rating
Based on mechanistic studies in cell lines and animal models (mice, rats), showing protein modifications and downstream effects.
Source
Crosstalk between Oxidative Stress and SIRT1: Impact on the Aging Process
Antero Salminen et al. · International Journal of Molecular Sciences · 2013
DOI 10.3390/ijms14023834
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