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Under energetic or cellular stress, AMPK activation relieves mTORC1-mediated inhibition of ULK1
PubMed Link Kadry MO
These factors induce EndMT through the activation of proinflammatory pathways and increasing oxidative stress, leading to endothelial dysfunction and plaque instability
Several methods are being studied to inhibit MMPs, which mediate TJ destruction and protect the BBB from ischemic injury
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