ArticleIndian journal of clinical biochemistry : IJCB2016
Hypoxia-Induced Inflammatory Chemokines in Subjects with a History of High-Altitude Pulmonary Edema.
Article in Indian journal of clinical biochemistry : IJCB, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- A severity-aware multi-agent soft actor-critic framework for medical resource coordination in plateau disaster rescue.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026Article
- Altitude hypoxia and hypoxemia: pathogenesis and management.Signal transduction and targeted therapy · 2026Review
- Eleutheroside E Attenuates Hypobaric Hypoxia-Induced High Altitude Pulmonary Edema by Regulating Ferritinophagy-Mediated Ferroptosis via Keap1-Nrf2 Regulatory Axis.Journal of inflammation research · 2026Article
- Hypobaric hypoxia can lead to an increase in lung dendritic cells and promote T-cell immunosuppression, thereby preventing the excessive progression of high-altitude pulmonary edema.Frontiers in immunology · 2026Article
- Understanding the mechanistic and therapeutic perspectives on cytokines and chemokines in acute high-altitude illness syndromes.Journal of pharmaceutical analysis · 2025Review
- Changes in Macrophages in Pulmonary Hypertension: A Focus on High-altitude Pulmonary Hypertension.Anatolian journal of cardiology · 2025Review
- Alternatively spliced NFKB1 transcripts enriched in Andean Aymara modulate inflammation, HIF and hemoglobin.Nature communications · 2025Article
- Review
- Inflammation in Pulmonary Hypertension and Edema Induced by Hypobaric Hypoxia Exposure.International journal of molecular sciences · 2022Review
- Genetic and immune changes in Tibetan high-altitude populations contribute to biological adaptation to hypoxia.Environmental health and preventive medicine · 2022Article
- Hypoxia and Inflammation: Insights From High-Altitude Physiology.Frontiers in physiology · 2021Review
- Andrographolide: Regulating the Master Regulator NF-κB.Indian journal of clinical biochemistry : IJCB · 2021Article
- Bidirectional Crosstalk Between Hypoxia Inducible Factors and Glucocorticoid Signalling in Health and Disease.Frontiers in immunology · 2021Review
- Subclinical elevated B-type Natriuretic Peptide (BNP) indicates endothelial dysfunction contributing to hypoxia susceptibility in healthy individuals.Life sciences · 2020Article
- Protective mechanism of fdft1 in steroid hormone synthesis pathway in SD rats with acute hypoxic injury.Genes & genomics · 2020Article
- Deregulated hypoxic response in myeloid cells: A model for high-altitude pulmonary oedema (HAPE).Acta physiologica (Oxford, England) · 2020Article
- Subclinical pulmonary dysfunction contributes to high altitude pulmonary edema susceptibility in healthy non-mountaineers.Scientific reports · 2017Article
- Chemokines in High Altitude Pulmonary Edema.Indian journal of clinical biochemistry : IJCB · 2016Article
- Neutrophil-lymphocyte ratio as an early predictive biomarker for severity in patients with high altitude pulmonary edema.Medical journal, Armed Forces IndiaArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High altitude hypoxia is known to induce an inflammatory response in immune cells. Hypoxia induced inflammatory chemokines may contribute to the development of high altitude pulmonary edema (HAPE) by causing damage to the lung endothelial cells and thereby capillary leakage. In the present study, we were interested to know whether chronic inflammation may contribute to HAPE susceptibility. We examined the serum levels of macrophage inflammatory protein-1α (MIP-1α), monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 in group (1) HAPE Susceptible subjects (n = 20) who had past history of HAPE and group (2) Control (n = 18) consist of subjects who had stayed at high altitude for 2 years without any history of HAPE. The data obtained confirmed that circulating MCP-1, MIP-1α were significantly upregulated in HAPE-S individuals as compared to the controls suggestive of chronic inflammation. However, it is not certain whether chronic inflammation is cause or consequence of previous episode of HAPE. The moderate systemic increase of these inflammatory markers may reflect considerable local inflammation. The existence of enhanced level of inflammatory chemokines found in this study support the hypothesis that subjects with past history of HAPE have higher baseline chronic inflammation which may contribute to HAPE susceptibility.
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