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[1] According to the researchers TGF-beta1 induction of angiogenesis requires a rapid and transient apoptotic effect mediated by VEGF/VEGFR2. AHK-Cu, by enhancing levels of the Vascular Endothelial Growth Factor, may possibly activate fibroblasts and endothelial cells

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Furthermore, a second mechanism involved would be related to TGF--dependent apoptotic processes, producing an increase in caspase 8, which in turn acts as an inducer of caspases 3, 6 and 7, giving rise to apoptosis [29,46]

The body interprets rapid fat loss as a significant stressor, releasing inflammatory mediators as part of the adaptive response

The longitudinal clinical study included two groups: a healthy control group with no trauma exposure and a trauma-exposed group, the latter consisting of individuals with a current PTSD diagnosis ( N = 41) and those with subclinical PTSD symptoms but no formal diagnosis ( N = 24, with a mean CAPS total score of 12.7)