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The role of autophagy in pulmonary hypertension: a double-edge sword

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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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Acknowledgements

We thank Adam Y. Xiao from Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport who helped us improve the writing. This project was supported by National Natural Science Foundation of China (81400208, 81670405, 81370409 and 81370408), Natural Foundation of Jiangsu Province (BK20161355) and Social Development Foundation of Zhenjiang (SH2016033) and Young Medical Talents of Jiangsu Province (QNRC2016835).

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Correspondence to Jinchuan Yan.

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Chen, R., Jiang, M., Li, B. et al. The role of autophagy in pulmonary hypertension: a double-edge sword. Apoptosis 23, 459–469 (2018). https://doi.org/10.1007/s10495-018-1477-4

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