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Reducing global inequities in medical oxygen access: the Lancet Global Health Commission on medical oxygen security
(Elsevier BV, 2025-03)
Hamish R Graham
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Carina King
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Ahmed Ehsanur Rahman
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Freddy Eric Kitutu
;
Leith Greenslade
Scopus© Citations 53 1
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Tumor hypoxia shapes natural killer cell anticancer activities
(Springer Science and Business Media LLC, 2025-05-30)
RETAMAL LUCERO, MAURICIO ANTONIO
;
Flavio Salazar-Onfray
;
Fermín E. González
;
Andrés Tittarelli
1
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Shifting from Hypoxia to Hyperoxia to Assess the Peripheral Chemosensory Drive of Ventilation
(0002)
Patricio Zapata
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Carolina Larraín
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Edison-Pablo Reyes
;
Ricardo Fernández
Scopus© Citations 2 3
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Connexins in Cancer, the Possible Role of Connexin46 as a Cancer Stem Cell-Determining Protein
(2023)
Isidora M. León-Fuentes
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María G. Salgado-Gil
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María S. Novoa
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RETAMAL LUCERO, MAURICIO ANTONIO
<jats:p>Cancer is a widespread and incurable disease caused by genetic mutations, leading to uncontrolled cell proliferation and metastasis. Connexins (Cx) are transmembrane proteins that facilitate intercellular communication via hemichannels and gap junction channels. Among them, Cx46 is found mostly in the eye lens. However, in pathological conditions, Cx46 has been observed in various types of cancers, such as glioblastoma, melanoma, and breast cancer. It has been demonstrated that elevated Cx46 levels in breast cancer contribute to cellular resistance to hypoxia, and it is an enhancer of cancer aggressiveness supporting a pro-tumoral role. Accordingly, Cx46 is associated with an increase in cancer stem cell phenotype. These cells display radio- and chemoresistance, high proliferative abilities, self-renewal, and differentiation capacities. This review aims to consolidate the knowledge of the relationship between Cx46, its role in forming hemichannels and gap junctions, and its connection with cancer and cancer stem cells.</jats:p>
Scopus© Citations 3 2
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Health Effects of Chronic Intermittent Hypoxia at a High Altitude among Chilean Miners: Rationale, Design, and Baseline Results of a Longitudinal Study
(2021)
Sergio Muñoz
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Carolina Nazzal
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Daniel Jimenez
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Patricia Frenz
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Patricia Flores
<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Objectives</jats:title> <jats:p>This study aims to assess the health effects on mining workers of exposure to chronic intermittent hypoxia (CIH) at high- and very high-altitude mining compared with similar work at lower altitudes in Chile, and it also aims to constitute the baseline of a 5-year follow-up study.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>We designed a cross-sectional study to assess health conditions in 483 miners working at 2 levels of altitude exposure: 336 working at a very high or high altitude (HA; 247 above 3900–4400 m, and 89 at 3000–3900 m), and 147 below 2400 m. Subjects were randomly selected in two stages. First, a selection of mines from a census of mines in each altitude stratum was made. Secondly, workers with less than 2 years of employment at each of the selected mines were recruited. The main outcomes measured at the baseline were mountain sickness, sleep alterations, hypertension, body mass index, and neurocognitive functions.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Prevalence of acute mountain sickness (AMS) was 28.4% in the very high-altitude stratum (P = 0.0001 compared with the low stratum), and 71.7% experienced sleep disturbance (P = 0.02). The adjusted odds ratio for AMS was 9.2 (95% confidence interval: 5.2–16.3) when compared with the very high- and low-altitude groups. Motor processing speed and spatial working memory score were lower for the high-altitude group. Hypertension was lower in the highest-altitude subjects, which may be attributed to preoccupational screening even though this was not statistically significant.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Despite longer periods of acclimatization to CIH, subjects continue to present AMS and sleep disturbance. Compromise of executive functions was detected, including working memory at HA. Further rigorous research is warranted to understand long-term health impacts of high-altitude mining, and to provide evidence-based policy recommendations.</jats:p> </jats:sec>
6Scopus© Citations 9
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Successful use of mild therapeutic hypothermia as compassionate treatment for severe refractory hypoxemia in COVID-19
(2021)
Pablo Cruces
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Camila Cores
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Daniel Casanova
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Federico Pizarro
;
Franco Díaz
2Scopus© Citations 13
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Fisura Labio Palatina. Revisión de la Literatura
(2022)
Ruth Prieto-Gómez
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Andrés Carreño
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Ammy Contreras
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Marco Garay
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Ignacio Labarca
1Scopus© Citations 3
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Caveolin-1-Mediated Tumor Suppression Is Linked to Reduced HIF1α S-Nitrosylation and Transcriptional Activity in Hypoxia
(2020)
Carlos Sanhueza
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CASTILLO BENNETT, JIMENA VICTORIA
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Manuel Valenzuela-Valderrama
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Pamela Contreras
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Lorena Lobos-González
<jats:p>Caveolin-1 (CAV1) is a well-established nitric oxide synthase inhibitor, whose function as a tumor suppressor is favored by, but not entirely dependent on, the presence of E-cadherin. Tumors are frequently hypoxic and the activation of the hypoxia-inducible factor-1α (HIF1α) promotes tumor growth. HIF1α is regulated by several post-translational modifications, including S-nitrosylation. Here, we evaluate the mechanisms underlying tumor suppression by CAV1 in cancer cells lacking E-cadherin in hypoxia. Our main findings are that CAV1 reduced HIF activity and Vascular Endothelial Growth Factor expression in vitro and in vivo. This effect was neither due to reduced HIF1α protein stability or reduced nuclear translocation. Instead, HIF1α S-nitrosylation observed in hypoxia was diminished by the presence of CAV1, and nitric oxide synthase (NOS) inhibition by Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) reduced HIF1α transcriptional activity in cells to the same extent as observed upon CAV1 expression. Additionally, arginase inhibition by (S)-(2-Boronoethyl)-L-cysteine (BEC) partially rescued cells from the CAV1-mediated suppression of HIF1α transcriptional activity. In vivo, CAV1-mediated tumor suppression was dependent on NOS activity. In summary, CAV1-dependent tumor suppression in the absence of E-cadherin is linked to reduced HIF1α transcriptional activity via diminished NOS-mediated HIF1α S-nitrosylation.</jats:p>
Scopus© Citations 10 1 3
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New Perspectives to Improve Mesenchymal Stem Cell Therapies for Drug-Induced Liver Injury
(2022)
EZQUER, EDUARDO FERNANDO
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HUANG, YA LIN
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EZQUER, EDUARDO MARCELO
<jats:p>Drug-induced liver injury (DILI) is one of the leading causes of acute liver injury. Many factors may contribute to the susceptibility of patients to this condition, making DILI a global medical problem that has an impact on public health and the pharmaceutical industry. The use of mesenchymal stem cells (MSCs) has been at the forefront of regenerative medicine therapies for many years, including MSCs for the treatment of liver diseases. However, there is currently a huge gap between these experimental approaches and their application in clinical practice. In this concise review, we focus on the pathophysiology of DILI and highlight new experimental approaches conceived to improve cell-based therapy by the in vitro preconditioning of MSCs and/or the use of cell-free products as treatment for this liver condition. Finally, we discuss the advantages of new approaches, but also the current challenges that must be addressed in order to develop safer and more effective procedures that will allow cell-based therapies to reach clinical practice, enhancing the quality of life and prolonging the survival time of patients with DILI.</jats:p>
Scopus© Citations 10 1
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Sustained Energy Deficit Following Perinatal Asphyxia: A Shift towards the Fructose-2,6-bisphosphatase (TIGAR)-Dependent Pentose Phosphate Pathway and Postnatal Development
(2021)
Carolyne Lespay-Rebolledo
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Andrea Tapia-Bustos
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Ronald Perez-Lobos
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Valentina Vio
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Emmanuel Casanova-Ortiz
<jats:p>Labor and delivery entail a complex and sequential metabolic and physiologic cascade, culminating in most circumstances in successful childbirth, although delivery can be a risky episode if oxygen supply is interrupted, resulting in perinatal asphyxia (PA). PA causes an energy failure, leading to cell dysfunction and death if re-oxygenation is not promptly restored. PA is associated with long-term effects, challenging the ability of the brain to cope with stressors occurring along with life. We review here relevant targets responsible for metabolic cascades linked to neurodevelopmental impairments, that we have identified with a model of global PA in rats. Severe PA induces a sustained effect on redox homeostasis, increasing oxidative stress, decreasing metabolic and tissue antioxidant capacity in vulnerable brain regions, which remains weeks after the insult. Catalase activity is decreased in mesencephalon and hippocampus from PA-exposed (AS), compared to control neonates (CS), in parallel with increased cleaved caspase-3 levels, associated with decreased glutathione reductase and glutathione peroxidase activity, a shift towards the TIGAR-dependent pentose phosphate pathway, and delayed calpain-dependent cell death. The brain damage continues long after the re-oxygenation period, extending for weeks after PA, affecting neurons and glial cells, including myelination in grey and white matter. The resulting vulnerability was investigated with organotypic cultures built from AS and CS rat newborns, showing that substantia nigra TH-dopamine-positive cells from AS were more vulnerable to 1 mM of H2O2 than those from CS animals. Several therapeutic strategies are discussed, including hypothermia; N-acetylcysteine; memantine; nicotinamide, and intranasally administered mesenchymal stem cell secretomes, promising clinical translation.</jats:p>
1Scopus© Citations 5

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