ROS Promote Ox-LDL-Induced Platelet Activation by Up-Regulating Autophagy Through the Inhibition of the PI3K/AKT/mTOR Pathway

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Population

In vitro platelets

Comparison

Treatment with oxidized low-density lipoprotein… vs Untreated platelets or alternative treatment…

Design

Preclinical

Authors

Discussion

Hypothesis-generating for ROS-autophagy targeting in oxLDL thrombosis; leaves open clinical relevance pending human trials.

Population

In vitro platelets

Intervention

Treatment with oxidized low-density lipoprotein (ox-LDL), N-acetylcysteine (NAC), rapamycin, and/or 3-MA

Comparator

Untreated platelets or alternative treatment combinations

Outcome

Platelet aggregation, adhesion, CD62p expression, ROS levels, and autophagy markers (LC3II/LC3I ratio, Beclin1, p62)surrogate

Inhibition of ROS production reduces autophagy and suppresses ox-LDL-induced platelet activation via the PI3K/AKT/mTOR pathway.

Wang et al. (2018) studied this question.

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