PMID- 34434114
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210827
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 12
DP  - 2021
TI  - Oxidative Stress, Kinase Activation, and Inflammatory Pathways Involved in 
      Effects on Smooth Muscle Cells During Pulmonary Artery Hypertension Under 
      Hypobaric Hypoxia Exposure.
PG  - 690341
LID - 10.3389/fphys.2021.690341 [doi]
LID - 690341
AB  - High-altitude exposure results in hypobaric hypoxia, which affects organisms by 
      activating several mechanisms at the physiological, cellular, and molecular 
      levels and triggering the development of several pathologies. One such pathology 
      is high-altitude pulmonary hypertension (HAPH), which is initiated through 
      hypoxic pulmonary vasoconstriction to distribute blood to more adequately 
      ventilated areas of the lungs. Importantly, all layers of the pulmonary artery 
      (adventitia, smooth muscle, and endothelium) contribute to or are involved in the 
      development of HAPH. However, the principal action sites of HAPH are pulmonary 
      artery smooth muscle cells (PASMCs), which interact with several extracellular 
      and intracellular molecules and participate in mechanisms leading to 
      proliferation, apoptosis, and fibrosis. This review summarizes the alterations in 
      molecular pathways related to oxidative stress, inflammation, kinase activation, 
      and other processes that occur in PASMCs during pulmonary hypertension under 
      hypobaric hypoxia and proposes updates to pharmacological treatments to mitigate 
      the pathological changes in PASMCs under such conditions. In general, PASMCs 
      exposed to hypobaric hypoxia undergo oxidative stress mediated by Nox4, 
      inflammation mediated by increases in interleukin-6 levels and inflammatory cell 
      infiltration, and activation of the protein kinase ERK1/2, which lead to the 
      proliferation of PASMCs and contribute to the development of hypobaric 
      hypoxia-induced pulmonary hypertension.
CI  - Copyright (c) 2021 Siques, Pena, Brito and El Alam.
FAU - Siques, Patricia
AU  - Siques P
AD  - Institute of Health Studies, Arturo Prat University, Iquique, Chile.
FAU - Pena, Eduardo
AU  - Pena E
AD  - Institute of Health Studies, Arturo Prat University, Iquique, Chile.
FAU - Brito, Julio
AU  - Brito J
AD  - Institute of Health Studies, Arturo Prat University, Iquique, Chile.
FAU - El Alam, Samia
AU  - El Alam S
AD  - Institute of Health Studies, Arturo Prat University, Iquique, Chile.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210809
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC8381601
OTO - NOTNLM
OT  - high altitude
OT  - hypobaric hypoxia
OT  - inflammation
OT  - kinases
OT  - oxidative stress
OT  - pulmonary artery smooth muscle cell
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/08/27 06:00
MHDA- 2021/08/27 06:01
PMCR- 2021/08/09
CRDT- 2021/08/26 06:09
PHST- 2021/04/02 00:00 [received]
PHST- 2021/07/16 00:00 [accepted]
PHST- 2021/08/26 06:09 [entrez]
PHST- 2021/08/27 06:00 [pubmed]
PHST- 2021/08/27 06:01 [medline]
PHST- 2021/08/09 00:00 [pmc-release]
AID - 10.3389/fphys.2021.690341 [doi]
PST - epublish
SO  - Front Physiol. 2021 Aug 9;12:690341. doi: 10.3389/fphys.2021.690341. eCollection 
      2021.