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. 2023 Jan;108(1):1-4.
doi: 10.1113/EP090967. Epub 2022 Nov 21.

On the mechanisms underlying activation and reversal of high altitude-induced pulmonary hypertension in humans - Another piece in the pulmonary puzzle

Marc Moritz Berger  1 , Damian Miles Bailey  2
Affiliations

On the mechanisms underlying activation and reversal of high altitude-induced pulmonary hypertension in humans - Another piece in the pulmonary puzzle

Marc Moritz Berger et al. Exp Physiol. 2023 Jan.
No abstract available

Keywords: Sherpa; endothelin; high altitude; hypoxia; hypoxic pulmonary vasoconstriction; nitric oxide; reactive oxygen species; vascular remodelling.

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Conflict of interest statement

D.M.B. is Chair of the Life Sciences Working Group and member of the Human Spaceflight and Exploration Science Advisory Committee to the European Space Agency and is a member of the Space Exploration Advisory Committee to the UK Space Agency. D.M.B. is affiliated to the companies FloTBI, BrainEx and OrgEx focused on the technological development of novel biomarkers of brain injury in humans.

Figures

FIGURE 1
FIGURE 1
Phases and mechanistic pathways underlying HPV in humans. In the first phase, hypoxia increases the production of free radicals and associated ROS (primarily superoxide anions and hydrogen peroxide) at complex III of the mitochondrial electron transport chain. After being released to the cytosol, superoxide is converted to hydrogen peroxide, which activates downstream targets that induce an increase in intracellular calcium concentration and contraction of pulmonary vascular smooth muscle cells (Smith & Schumacker, 2019). Vasoconstriction is subsequently maintained by a reduction in vascular NO bioavailability combined with an elevation in the circulating concentration of endothelium‐derived vasoconstrictors (Bailey et al., ; Dunham‐Snary et al., 2017). If HPV is maintained, HIF‐1α activates a complex signalling cascade, ultimately inducing pulmonary vascular remodelling and fixation of HPV (Smith & Schumacker, 2019). Abbreviations: ET‐1, endothelin‐1; HIF‐1α, hypoxia‐inducible factor‐1α; HPV, hypoxic pulmonary vasoconstriction; PASMCs, pulmonary arterial smooth muscle cells; ROS, reactive oxygen species
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References

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Publication types

Supplementary concepts