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| http://dx.doi.org/10.1136/jnnp.2004.036962 | DOI Listing |
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Cardiology Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA. (X.Z., Q.X., A.V., Z.L.).
Background: Recent studies show that hyperactivation of mTOR (mammalian target of rapamycin) signaling plays a causal role in the development of thoracic aortic aneurysm and dissection. Modulation of PP2A (protein phosphatase 2A) activity has been shown to be of significant therapeutic value. In light of the effects that PP2A can exert on the mTOR pathway, we hypothesized that PP2A activation by small-molecule activators of PP2A could mitigate AA progression in Marfan syndrome (MFS).
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A 69-year-old man with chest pain was diagnosed with acute type B aortic dissection with the entry tear located at distal arch and a distal aortic arch aneurysm. Therefore, we performed debranching thoracic endovascular aortic repair 2 weeks after type B aortic dissection onset. First, the graft was anastomosed to bilateral axillary arteries.
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The underlying mechanisms of abdominal aortic aneurysms (AAAs) are not fully understood. Given the multifactorial nature of AAA development and progression, a comprehensive approach is essential. Throughout my academic career, I conducted various studies on AAA.
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