1159-1170 April 12, 2013

Chloroquine Prevents Progression of Experimental
Pulmonary Hypertension via Inhibition of Autophagy and
Lysosomal Bone Morphogenetic Protein Type II Receptor
DegradationNovelty and Significance
by Lu Long, Xudong Yang, Mark Southwood, Junyu Lu, Stefan J. Marciniak,
Benjamin J. Dunmore, and Nicholas W. Morrell
Circulation Research
Volume 112(8):1159-1170
April 12, 2013
Copyright © American Heart Association, Inc. All rights reserved.
Chloroquine attenuates monocrotaline-induced pulmonary hypertension.
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.
Chloroquine partially inhibits the progression of established pulmonary hypertension in the
monocrotaline (MCT) model.
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.
Autophagy markers are increased in monocrotaline (MCT)-exposed rat lung.
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.
Chloroquine restores defective bone morphogenetic protein (BMP) signaling in monocrotaline
(MCT)-exposed rat lung.
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.
Chloroquine induces autophagy marker expression in rat pulmonary microvascular smooth
muscle cells.
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.
Chloroquine inhibits cell proliferation and induces apoptosis in rat pulmonary artery smooth
muscle cells (PASMCs).
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.
Knockdown of ATG5 inhibited pulmonary artery smooth muscle cells (PASMCs) proliferation.
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.
A schematic representation of proposed mechanism for the role of chloroquine in
monocrotaline-induced pulmonary hypertension.
Lu Long et al. Circ Res. 2013;112:1159-1170
Copyright © American Heart Association, Inc. All rights reserved.