ArticleBMC cardiovascular disorders2025
Mechanism of adenosine monophosphate-activated protein kinase promoting lower extremity varicose veins development via cytoskeletal dynamics.
Article in BMC cardiovascular disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThis study aimed to investigate the potential involvement of 5'-AMP-activated protein kinase (AMPK) in the pathogenesis of lower-extremity varicose veins (VV).
methodsIn this study, 8 patients with CEAP stage C6 chronic venous disease and 8 age-matched healthy controls were prospectively recruited to collect samples for preparation of subsequent experiments.None of the patients included in the molecular analyses were diagnosed with diabetes, as our analysis of 73,313 patients demonstrated that diabetes is generally not associated with VV. Western blotting was employed to quantify the levels of p-AMPK, G-actin, p-tubulin, p-HSP20, and 14-3-3 proteins in each sample.
resultsEpidemiological analyses revealed 5,262 patients with VVs among 714,789 inpatients. Of these patients, only 351 VV patients were diagnosed with type 2 DM, while 4,911 were not diagnosed with DM. Higher levels of AMPK activation were evident in VV samples in molecular analyses, with the p-AMPK level in the VV group being 1.98 ± 0.56 times higher than that in the NV group (n = 3, P < 0.001). G-actin levels in VV samples were additionally 2.14 ± 0.60 times higher than those in NV samples (n = 3, P < 0.001). Increased cofilin activation was also observed in VV samples, as evidenced by p-cofilin levels in the VV group that were 0.63 ± 0.10 times those in the NV group (n = 3, P < 0.001), with VV samples additionally exhibiting p-HSP20 levels that were 2.02 ± 0.59 times higher than those in NV samples (n = 3, P < 0.001).
conclusionThese results suggest that AMPK Is likely to be involved lower extremity VV development, potentially by inducing vasodilation through the dysregulation of F-actin cytoskeletal dynamics in VSMCs, increasing cofilin activation, the displacement of which from 14-3-3 can lead to dephosphorylation mediated by HSP20,and then causes its dephosphorylation and increased activity, and thereby reducing cytoskeletal actin homeostasis and promoting vascular relaxation.These findings elucidate the possible regulatory role of AMPK phosphorylation in vein wall degeneration and provide a theoretical basis for further studies.
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