PMID- 26448276
DCOM- 20161213
LR  - 20161230
IS  - 1533-4023 (Electronic)
IS  - 0160-2446 (Linking)
VI  - 67
IP  - 2
DP  - 2016 Feb
TI  - Signal Mechanisms of Vascular Remodeling in the Development of Pulmonary Arterial
PG  - 182-90
LID - 10.1097/FJC.0000000000000328 [doi]
AB  - Pulmonary artery hypertension (PAH) is a chronic progressive disease
      characterized by persistent elevation of pulmonary arterial vascular pressure.
      The disease severely limits the function of the right ventricle, causing organ
      failure and finally leading to death. Despite significant advances in
      pharmacological treatments, PAH remains an incurable disease with high morbidity 
      and mortality. The histopathological change of PAH is featured by remodeling of
      the pulmonary vascular. Abnormal proliferation of pulmonary artery smooth muscle 
      cells in peripheral vascular is 1 major pathological finding of pulmonary
      vascular remodeling. Current therapeutics available for PAH primarily aim at
      inhibiting the pulmonary vasoconstriction and resisting pulmonary vascular
      remodeling. To date, only some inhibitors targeting proliferative signaling
      pathways have been used to suppress the proliferation of pulmonary artery smooth 
      muscle cells and reverse pulmonary vascular remodeling. However, because of
      serious side effects, their clinical use is limited, and more validation is
      needed before the inhibitors can be transferred into clinical use. This review
      will focus on signal mechanisms of vascular remodeling in the development of PAH 
      and give an overview of recent advances in research on inhibitors targeting
      proliferative pathways.
FAU - Li, Ming-xing
AU  - Li MX
AD  - *Department of Pharmacy, Zhu Jiang Hospital, Southern Medical University,
      Guangzhou, China; daggerDepartment of Biopharmaceutical, Yulin Normal University,
      Yulin, China; and double daggerDepartment of Clinical Pharmacy, Guangzhou
      Hospital of Integrated Traditional and West Medicine, Guangzhou, China.
FAU - Jiang, De-qi
AU  - Jiang DQ
FAU - Wang, Yan
AU  - Wang Y
FAU - Chen, Qing-zhuang
AU  - Chen QZ
FAU - Ma, Yan-jiao
AU  - Ma YJ
FAU - Yu, Shan-shan
AU  - Yu SS
FAU - Wang, Yong
AU  - Wang Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Animals
MH  - DNA Damage/physiology
MH  - Humans
MH  - Hypertension, Pulmonary/*metabolism/*pathology
MH  - Inflammation Mediators/metabolism
MH  - Muscle, Smooth, Vascular/metabolism/pathology
MH  - Pulmonary Artery/*metabolism/*pathology
MH  - Signal Transduction/*physiology
MH  - Vascular Remodeling/*physiology
EDAT- 2015/10/09 06:00
MHDA- 2016/12/15 06:00
CRDT- 2015/10/09 06:00
PHST- 2015/10/09 06:00 [entrez]
PHST- 2015/10/09 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - 10.1097/FJC.0000000000000328 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 2016 Feb;67(2):182-90. doi: 10.1097/FJC.0000000000000328.