Research
Hormonal
Genetic deletion or silencing of the adaptor protein p66Shc reduces oxidative stress, improves endothelial function, and reduces stroke size in animal models, but may increase infarct size in specific myocardial ischemia-reperfusion contexts.
Current research suggests that targeting p66Shc could help prevent stroke and vascular aging, but it is not yet a viable therapeutic strategy due to conflicting effects on heart tissue. Focus on proven lifestyle factors like exercise and diet to manage oxidative stress.
ModerateQualifiesMEDIUM confidence
In p66Shc-/- mice, levels of intracellular ROS are reduced as is oxidative damage of DNA and proteins... p66Shc-/- mice display decreased production of free radicals in the brain and systemically and have smaller strokes... genetic deletion or in vivo silencing of p66Shc is associated with larger infarcts after 30 min of occlusion of the left anterior descending artery followed by 24 h of reperfusion.
Why this rating
Strong animal data with conflicting results depending on the tissue (brain vs. heart) and ischemia duration.
Source
Molecular mechanism of endothelial and vascular aging: implications for cardiovascular disease
Giovanni G. Camici et al. · European Heart Journal · 2015
DOI 10.1093/eurheartj/ehv587
narrative_reviewCited 226×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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