Abstract
Autophagy is a recycling process that degrades damaged or unneeded cellular components for renewal. Accumulating evidence suggests that dysregulation of autophagy is involved in pulmonary hypertension (PH). PH is a progressive disease characterized by persistent proliferation of apoptosis-resistant pulmonary vascular cells. However, reports on the role of autophagy in the development of PH are often conflicting. In this review, we discuss recent development in the field with emphasis on pulmonary arterial endothelial cells, pulmonary smooth muscle cells, right ventricular myocyte, as well as pharmacological strategies targeting the autophagic signaling pathway.
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