Synopsis

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

AMP-activated protein kinase (AMPK) is a key cellular energy sensor that regulates glucose and lipid metabolism. In recent years, increasing scientific evidence has linked AMPK activation to protective effects in diabetic retinopathy (DR), a common and vision-threatening complication of diabetes. Preclinical studies using animal models and cell cultures have shown that AMPK activation can reduce retinal inflammation, oxidative stress, and vascular leakage—processes that are central to the pathogenesis of DR. For example, pharmacological activators of AMPK, such as metformin and AICAR, have demonstrated the ability to inhibit retinal vascular endothelial growth factor (VEGF) expression and suppress inflammatory cytokine production, thereby protecting retinal cells from hyperglycemia-induced damage. Additionally, AMPK activation appears to modulate tight junction proteins, reducing blood-retinal barrier breakdown. While these findings are promising, most of the evidence is preclinical, with only limited clinical data directly linking AMPK activation to improved outcomes in DR patients. Nevertheless, the use of AMPK activators like metformin in diabetic individuals has been associated with reduced incidence or progression of DR in some observational studies. In summary, while the current body of evidence is not yet robust enough for unequivocal clinical recommendations, there is a sound scientific rationale and moderate preclinical support for targeting AMPK in the management of diabetic retinopathy.

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