Synopsis

Source of validity: Scientific
Rating (out of 5): 3

AMP-activated protein kinase (AMPK) is an enzyme that acts as a central regulator of cellular energy homeostasis. Its activation has been extensively studied in the context of metabolic diseases, including atherosclerosis (a form of arteriosclerosis). Scientific evidence supports the potential of AMPK activation to mitigate processes involved in arteriosclerosis, such as endothelial dysfunction, inflammation, and lipid accumulation. Animal and cell culture studies have demonstrated that pharmacological activation of AMPK can inhibit vascular smooth muscle cell proliferation, suppress inflammatory responses in vascular tissue, and enhance cholesterol efflux from macrophages, thereby reducing foam cell formation—an early event in atherosclerotic plaque development.

Additionally, some widely used anti-diabetic drugs, such as metformin, exert part of their beneficial cardiovascular effects through AMPK activation. Human observational and interventional studies suggest an association between AMPK activity and reduced cardiovascular events, but direct clinical trials targeting AMPK for arteriosclerosis are limited. Thus, while preclinical data and some indirect clinical evidence support AMPK as a promising target in arteriosclerosis prevention and treatment, more robust clinical trials are needed to fully establish its efficacy in humans. Overall, the scientific rationale for AMPK’s use in arteriosclerosis is strong, but clinical validation is still emerging, justifying a moderate evidence rating.

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