Key result
Autophagy dysregulation drives vascular pathology, including atherosclerosis, calcification, and pulmonary hypertension.
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There is increasing interest in the role of autophagic flux in maintaining normal vessel wall biology and a growing suspicion that autophagic dysregulation may be a common pathway through which vascular aging and associated pathologies develop. Within endothelial and smooth muscle cells, diverse but important triggers that range from oxidized lipids to β-amyloid seem to stimulate autophagosome formation potently. In addition, emerging evidence links autophagy to a wide array of vascular processes ranging from angiogenesis to calcification of the vessel wall. Alterations in autophagic flux are also increasingly being implicated in disease processes that include both atherosclerosis and pulmonary hypertension. Finally, recent insights point toward an important role of autophagy in the paracrine regulation of vasoactive substances from the endothelium. Here, we review the progress in understanding how autophagy can contribute to vascular biology and the emerging strategies to target this process for therapeutic benefit.
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Nussenzweig et al. (2015) conducted a review in Vascular aging, atherosclerosis, and pulmonary hypertension. Autophagy / autophagic flux was evaluated. Autophagy regulates vascular processes including angiogenesis and vessel calcification, with dysregulation implicated in atherosclerosis and pulmonary hypertension.
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