ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2020
Increased hypoxic proliferative response and gene expression in erythroid progenitor cells of Andean highlanders with chronic mountain sickness.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- High‑altitude polycythemia: Unveiling the molecular landscape beyond erythropoietin (Review).International journal of molecular medicine · 2026Review
- Altitude hypoxia and hypoxemia: pathogenesis and management.Signal transduction and targeted therapy · 2026Review
- Advances in Understanding Adaptive Hemoglobin Concentration at High Altitude.American journal of human biology : the official journal of the Human Biology Council · 2025Article
- Life destiny of erythrocyte in high altitude erythrocytosis: mechanisms underlying the progression from physiological (moderate) to pathological (excessive) high-altitude erythrocytosis.Frontiers in genetics · 2025Review
- [Progress in multiomics research on high altitude polycythemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024Review
- Altitude illnesses.Nature reviews. Disease primers · 2024Review
- Long noncoding RNA HIKER regulates erythropoiesis in Monge's disease via CSNK2B.The Journal of clinical investigation · 2023Article
- Arginine attenuates chronic mountain sickness in rats via microRNA-144-5p.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Article
- Preserved peak exercise capacity in Andean highlanders with excessive erythrocytosis both before and after isovolumic hemodilution.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- High-Altitude Erythrocytosis: Mechanisms of Adaptive and Maladaptive Responses.Physiology (Bethesda, Md.) · 2022Review
- [Expression of MMP-9 and microvessels in rat organs with chronic mountain sickness].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2021Article
- Protective role of estrogen against excessive erythrocytosis in Monge's disease.Experimental & molecular medicine · 2021Article
- Stroke-Related Mortality at Different Altitudes: A 17-Year Nationwide Population-Based Analysis From Ecuador.Frontiers in physiology · 2021Article
- Excessive Erythrocytosis and Chronic Mountain Sickness in Dwellers of the Highest City in the World.Frontiers in physiology · 2020Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Excessive erythrocytosis (EE) is the main sign of chronic mountain sickness (CMS), a maladaptive clinical syndrome prevalent in Andean and other high-altitude populations worldwide. The pathophysiological mechanism of EE is still controversial, as physiological variability of systemic respiratory, cardiovascular, and hormonal responses to chronic hypoxemia complicates the identification of underlying causes. Induced pluripotent stem cells derived from CMS highlanders showed increased expression of genes relevant to the regulation of erythropoiesis, angiogenesis, cardiovascular, and steroid-hormone function that appear to explain the exaggerated erythropoietic response. However, the cellular response to hypoxia in native CMS cells is yet unknown. This study had three related aims: to determine the hypoxic proliferation of native erythroid progenitor burst-forming unit-erythroid (BFU-E) cells derived from CMS and non-CMS peripheral blood mononuclear cells; to examine their sentrin-specific protease 1 (SENP1), GATA-binding factor 1 (GATA1), erythropoietin (EPO), and EPO receptor (EPOR) expression; and to investigate the functional upstream role of SENP1 in native progenitor differentiation into erythroid precursors. Native CMS BFU-E colonies showed increased proliferation under hypoxic conditions compared with non-CMS cells, together with an upregulated expression of SENP1, GATA1, EPOR; and no difference in EPO expression. Knock-down of the SENP1 gene abolished the augmented proliferative response. Thus, we demonstrate that native CMS progenitor cells produce a larger proportion of erythroid precursors under hypoxia and that SENP1 is essential for proliferation. Our findings suggest a significant intrinsic component for developing EE in CMS highlanders at the cellular and gene expression level that could be further enhanced by systemic factors such as alterations in respiratory control, or differential hormonal patterns.
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