Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure
Exposure to high altitudes generates a decrease in the partial pressure of oxygen, triggering a hypobaric hypoxic condition. This condition produces pathophysiologic alterations in an organism. In the lung, one of the principal responses to hypoxia is the development of hypoxic pulmonary vasoconstri...
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-10-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/20/12656 |
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| author | Samia El Alam Eduardo Pena Diego Aguilera Patricia Siques Julio Brito |
| author_facet | Samia El Alam Eduardo Pena Diego Aguilera Patricia Siques Julio Brito |
| author_sort | Samia El Alam |
| collection | DOAJ |
| description | Exposure to high altitudes generates a decrease in the partial pressure of oxygen, triggering a hypobaric hypoxic condition. This condition produces pathophysiologic alterations in an organism. In the lung, one of the principal responses to hypoxia is the development of hypoxic pulmonary vasoconstriction (HPV), which improves gas exchange. However, when HPV is exacerbated, it induces high-altitude pulmonary hypertension (HAPH). Another important illness in hypobaric hypoxia is high-altitude pulmonary edema (HAPE), which occurs under acute exposure. Several studies have shown that inflammatory processes are activated in high-altitude illnesses, highlighting the importance of the crosstalk between hypoxia and inflammation. The aim of this review is to determine the inflammatory pathways involved in hypobaric hypoxia, to investigate the key role of inflammation in lung pathologies, such as HAPH and HAPE, and to summarize different anti-inflammatory treatment approaches for these high-altitude illnesses. In conclusion, both HAPE and HAPH show an increase in inflammatory cell infiltration (macrophages and neutrophils), cytokine levels (IL-6, TNF-α and IL-1β), chemokine levels (MCP-1), and cell adhesion molecule levels (ICAM-1 and VCAM-1), and anti-inflammatory treatments (decreasing all inflammatory components mentioned above) seem to be promising mitigation strategies for treating lung pathologies associated with high-altitude exposure. |
| first_indexed | 2024-03-09T20:04:41Z |
| format | Article |
| id | doaj.art-4be51221495148dfbb8900b5de4390b7 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T20:04:41Z |
| publishDate | 2022-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-4be51221495148dfbb8900b5de4390b72023-11-24T00:34:54ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-10-0123201265610.3390/ijms232012656Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia ExposureSamia El Alam0Eduardo Pena1Diego Aguilera2Patricia Siques3Julio Brito4Institute of Health Studies, Arturo Prat University, Iquique 1100000, ChileInstitute of Health Studies, Arturo Prat University, Iquique 1100000, ChileInstitute of Health Studies, Arturo Prat University, Iquique 1100000, ChileInstitute of Health Studies, Arturo Prat University, Iquique 1100000, ChileInstitute of Health Studies, Arturo Prat University, Iquique 1100000, ChileExposure to high altitudes generates a decrease in the partial pressure of oxygen, triggering a hypobaric hypoxic condition. This condition produces pathophysiologic alterations in an organism. In the lung, one of the principal responses to hypoxia is the development of hypoxic pulmonary vasoconstriction (HPV), which improves gas exchange. However, when HPV is exacerbated, it induces high-altitude pulmonary hypertension (HAPH). Another important illness in hypobaric hypoxia is high-altitude pulmonary edema (HAPE), which occurs under acute exposure. Several studies have shown that inflammatory processes are activated in high-altitude illnesses, highlighting the importance of the crosstalk between hypoxia and inflammation. The aim of this review is to determine the inflammatory pathways involved in hypobaric hypoxia, to investigate the key role of inflammation in lung pathologies, such as HAPH and HAPE, and to summarize different anti-inflammatory treatment approaches for these high-altitude illnesses. In conclusion, both HAPE and HAPH show an increase in inflammatory cell infiltration (macrophages and neutrophils), cytokine levels (IL-6, TNF-α and IL-1β), chemokine levels (MCP-1), and cell adhesion molecule levels (ICAM-1 and VCAM-1), and anti-inflammatory treatments (decreasing all inflammatory components mentioned above) seem to be promising mitigation strategies for treating lung pathologies associated with high-altitude exposure.https://www.mdpi.com/1422-0067/23/20/12656inflammationhigh altitudepulmonary edemapulmonary hypertensionhypoxia |
| spellingShingle | Samia El Alam Eduardo Pena Diego Aguilera Patricia Siques Julio Brito Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure International Journal of Molecular Sciences inflammation high altitude pulmonary edema pulmonary hypertension hypoxia |
| title | Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure |
| title_full | Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure |
| title_fullStr | Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure |
| title_full_unstemmed | Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure |
| title_short | Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure |
| title_sort | inflammation in pulmonary hypertension and edema induced by hypobaric hypoxia exposure |
| topic | inflammation high altitude pulmonary edema pulmonary hypertension hypoxia |
| url | https://www.mdpi.com/1422-0067/23/20/12656 |
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