bims-oxygme Biomed News
on Oxygen metabolism
Issue of 2025–04–20
nine papers selected by
Onurkan Karabulut, Berkeley City College



  1. BMC Genomics. 2025 Apr 18. 26(1): 385
      Hypoxia often has negative effects on testis development and spermatogenesis of mammals. Plateau yaks have lived in the hypoxia environment for generations, but have ensured testicular function, which is closely related to their unique hypoxia response mechanism. Glucose metabolic reprogramming is an important way for cells to respond to stressful environments, especially the metabolite lactate, which is the energy basis for the development and differentiation of germ cells. In this study, hypoxia (5% O2) effectively promoted yak Sertoli cell proliferation and decreased autophagy and apoptosis. It was found that the cells showed good hypoxic adaptation. Metabolomics results showed that glucose metabolism was enhanced in yak Sertoli cells in response to hypoxia, and 13 glucose metabolites were increased, including the production and transport level of lactic acid (LA), which may have changed the pentose phosphate metabolic pathway of cells, these changes are conducive to support the glucose metabolism balance of cells under hypoxia. Crucially, when autophagy is activated under hypoxia, GLUT3, GLUT8, and MCT4 proteins are degraded, while GLUT1 and MCT1 are not affected, suggesting that autophagy may achieve glucose metabolic reprogramming by selectively regulating the expression of functional factors of glucose metabolism, which is conducive to energy intake and spermatogenesis in testis of yaks.
    Keywords:  Autophagy; Hypoxia; Metabolism reprogramming; Sertoli cells; Yak
    DOI:  https://doi.org/10.1186/s12864-025-11497-x
  2. Drug Test Anal. 2025 Apr 13.
      Pharmacological potential of Hypoxen, previously registered as Olifen is evaluated herein. Hypoxen is categorized as antihypoxic agent. The active substance is polydihydroxyphenylene thiosulfonate sodium. Human studies are limited and no clinical trials following international standards is available. There is however a developed body of knowledge emerging from original studies conducted by the Russian Military Medical Academy in 1980s and 1990s despite limited online access. Hypoxen is promoted to improve oxygen supply or reduce oxygen consumption under hypoxic conditions and physical load. It is thought to support faster recovery, and can be used in complex treatments of diseases accompanied by hypoxia like myocardial ischemia. From clinical perspective, it may enhance cellular respiration by improving coupling in the respiratory chain/accelerating oxidative phosphorylation, but also inhibit succinate dehydrogenase (SDH), and activate mitochondrial ATP-sensitive potassium channels (mitoKATP) in skeletal muscles and myocardium. In 2023, the World Anti-Doping Agency (WADA) added Hypoxen to the Monitoring Program as there had been documented evidence of its use by athletes. On in vitro experiments compared the influence of Hypoxen on oxidative phosphorylation with mitochondrial uncoupling agent 2,4-dinitrophenol (DNP) a unique metabolic modulator that strongly accelerates the metabolism rate, prohibited since 2024 by WADA. Most studies focus on exercise performance, and may provide some evidence that Hypoxen has the potential to enhance performance, the first criteria considered for addition of substance to the WADA Prohibited List. Pharmacodynamics and ergogenic effects of Hypoxen suggests potential as metabolic modulator.
    Keywords:  actoprotector; artificial redox systems; ergogenic aid; hypoxia; oxidative phosphorylation; oxygenation
    DOI:  https://doi.org/10.1002/dta.3887
  3. Med Gas Res. 2025 Sep 01. 15(3): 427-434
      Cardiovascular diseases remain the leading cause of death worldwide, underscoring the urgent need for additional therapeutic strategies to reduce their mortality rates. This review systematically outlines the historical development and recent advances of hyperbaric oxygen therapy in cardiovascular diseases, with a focus on its therapeutic mechanisms and clinical outcomes. Hyperbaric oxygen therapy enhances oxygen delivery to ischemic and reperfused tissues, promotes angiogenesis, and significantly suppresses oxidative stress, inflammatory cascades, and cardiomyocyte apoptosis, demonstrating multifaceted therapeutic potential in cardiovascular conditions. Specifically, hyperbaric oxygen therapy combined with reperfusion strategies has been shown to markedly improve left ventricular ejection fraction in acute myocardial infarction. In heart failure, it facilitates myocardial repair and enhances cardiac function. For arrhythmias, hyperbaric oxygen therapy effectively reduces the frequency and duration of premature ventricular contractions and paroxysmal tachycardia, while mitigating the risk of neurological complications following atrial fibrillation ablation. Furthermore, hyperbaric oxygen therapy preconditioning in cardiac surgery has demonstrated improvements in left ventricular stroke work, reductions in postoperative myocardial injury, and a decrease in related complications. Despite its promising applications, the widespread adoption of hyperbaric oxygen therapy remains hindered by the lack of standardized treatment protocols and high-quality evidence from rigorous clinical trials. In conclusion, this review underscores the potential value of hyperbaric oxygen therapy in the cardiovascular domain while highlighting the need for further optimization of therapeutic parameters and exploration of its synergistic effects with conventional therapies to provide clearer guidance for clinical implementation.
    Keywords:  acute myocardial infarction; anti-apoptosis; anti-inflammation; anti-oxidation; arrhythmias; cardiac rehabilitation; coronary artery bypass grafting; heart failure; hyperbaric oxygen therapy
    DOI:  https://doi.org/10.4103/mgr.MEDGASRES-D-24-00107
  4. PLoS Comput Biol. 2025 Apr 16. 21(4): e1012735
      The tumor microenvironment aids cancer progression by promoting several cancer hallmarks, independent of cancer-related mutations. Biophysical properties of this environment, such as the stiffness of the matrix cells adhere to and local cell density, impact proliferation, apoptosis, and the epithelial to mesenchymal transition (EMT). The latter is a rate-limiting step for invasion and metastasis, enhanced in hypoxic tumor environments but hindered by soft matrices and/or high cell densities. As these influences are often studied in isolation, the crosstalk between hypoxia, biomechanical signals, and the classic EMT driver TGF-β is not well mapped, limiting our ability to predict and anticipate cancer cell behaviors in changing tumor environments. To address this, we built a Boolean regulatory network model that integrates hypoxic signaling with a mechanosensitive model of EMT, which includes the EMT-promoting crosstalk of mitogens and biomechanical signals, cell cycle control, and apoptosis. Our model reproduces the requirement of Hif-1α for proliferation, the anti-proliferative effects of strong Hif-1α stabilization during hypoxia, hypoxic protection from anoikis, and hypoxia-driven mechanosensitive EMT. We offer experimentally testable predictions about the effect of VHL loss on cancer hallmarks, with or without secondary oncogene activation. Taken together, our model serves as a predictive framework to synthesize the signaling responses associated with tumor progression and metastasis in healthy vs. mutant cells. Our single-cell model is a key step towards more extensive regulatory network models that cover damage-response and senescence, integrating most cell-autonomous cancer hallmarks into a single model that can, in turn, control the behavior of in silico cells within a tissue model of epithelial homeostasis and carcinoma.
    DOI:  https://doi.org/10.1371/journal.pcbi.1012735
  5. Mol Neurobiol. 2025 Apr 14.
      Remote ischemic postconditioning (RIPostC) is known to improve motor function recovery in animal models, but its efficacy in alleviating cognitive impairment caused by ischemic stroke remains unclear. This study aims to investigate the beneficial role of RIPostC in recovering cognitive impairment induced by cerebral ischemia-reperfusion injury (CIRI). Building upon our previous research findings, we proved that the TK/BK/B2R pathway is crucial for understanding the crosstalk between cognitive impairment and RIPostC. Additionally, in vitro experiments were conducted using the oxygen glucose deprivation/re-oxygenation (OGD/r) HT-22 cell model, which revealed that the mechanism by which RIPostC suppressed mitochondrial apoptosis was mainly through the activation of the B2R/PI3K/AKT signaling pathway, thereby protecting neurons in the ischemic hippocampus from ischemic damage. To investigate the effect of RIPostC on cognitive function recovery following ischemic stroke, we established a rat model using left middle cerebral artery occlusion reperfusion (MCAO/r). 48 h after MCAO/r, rats were subjected to 3 circles of RIPostC therapy daily for 12 consecutive days. HOE140 was used to antagonize the bradykinin 2 receptor (B2R). Cognitive function was assessed using a modified neurological severity score, the Morris water maze, and the novel object recognition test. Local infarct volume in the hippocampus was measured through MRI scanning. The apoptosis rate of hippocampal neurons was quantified using TUNEL staining. Protein expression levels of kallikrein (TK) and mitochondrial apoptosis-related proteins, Cyt c, Bcl-2, Bax, cleaved caspase-3, and cleaved caspase-9, were detected in ischemic hippocampal tissue using Western blot (WB). The expression of bradykinin (BK) in serum and the ischemic penumbra was measured using an enzyme-linked immunosorbent (ELISA) assay. In the cell experiments, the HT-22 cell line and OGD/r model were used to simulate in vitro hippocampal ischemia. WB was performed to detect the expression of apoptosis-related proteins and PI3K/AKT pathway proteins. The apoptosis rate of HT-22 cells was detected using Annexin-V/PI flow cytometry and a cell viability kit. JC-1 staining and reactive oxygen species staining were used to evaluate mitochondrial condition. The PI3K/AKT pathway was inhibited using LY294002. RIPostC significantly upregulated the concentrations of TK and BK in the ischemic hippocampus. Behavioral function tests demonstrated that daily RIPostC therapy for 12 days significantly promoted cognitive function recovery in MCAO/r rats. Through MRI analysis, we found that RIPostC therapy effectively reduced the infarct volume in the hippocampus. Additionally, TUNEL staining and WB results of apoptosis-related proteins showed that RIPostC therapy significantly reduced apoptosis of hippocampal neurons. However, the therapeutic effect of RIPostC was reversed by the B2R antagonist HOE14, indicating that the TK/BK/B2R pathway mediated the neuroprotective effect of RIPostC. Cell experiments further confirmed that BK/B2R significantly attenuated mitochondrial apoptosis induced by ischemia-hypoxia injury in HT-22 cells. In vivo and in vitro results from WB demonstrated that the BK/B2R pathway activated the PI3K/AKT signaling pathway. Finally, the PI3K inhibitor LY294002 reversed the anti-apoptotic effect induced by BK/B2R. RIPostC therapy effectively inhibited mitochondrial apoptosis of hippocampal neurons and significantly alleviated cognitive dysfunction associated with CIRI by regulating the TK/BK/B2R-medated PI3K/AKT pathway. In conclusion, RIPostC represents a promising therapeutic strategy for combating cognitive dysfunction by inhibiting cell apoptosis in hippocampus. Moreover, our results suggest that RIPostC may have a broader protective effect against apoptosis in other ischemia-reperfusion-related diseases.
    Keywords:  Apoptosis; Cerebral ischemia–reperfusion injury; Cognitive dysfunction; Hippocampus; Remote ischemic postconditioning
    DOI:  https://doi.org/10.1007/s12035-025-04864-y
  6. Am J Physiol Cell Physiol. 2025 Apr 17.
      Cardiovascular diseases are associated with an altered cardiomyocyte metabolism. Due to a shortage of human heart tissue, experimental studies mostly rely on alternative approaches including animal and cell culture models. Since the use of isolated primary cardiomyocytes is limited, immortalized cardiomyocyte cell lines may represent a useful tool as they closely mimic human cardiomyocytes. This study is focused on the AC16 cell line generated from adult human ventricular cardiomyocytes. Despite an increasing number of articles employing AC16 cells, the comprehensive proteomic, bioenergetic and oxygen-sensing characterization of proliferating versus differentiated cells is still lacking. Here, we provide a comparison of these two stages, particularly emphasizing cell metabolism, mitochondrial function, and hypoxic signalling. The label-free quantitative mass spectrometry revealed a decrease in autophagy and cytoplasmic translation in differentiated AC16, confirming their phenotype. Cell differentiation led to the global increase in mitochondrial proteins (e.g. OXPHOS proteins, TFAM, VWA8, etc.) reflected by elevated mitochondrial respiration. Fatty acid oxidation proteins were increased in differentiated cells, while the expression levels of proteins associated with fatty acid synthesis were unchanged, and glycolytic proteins were decreased. There was a profound difference between proliferating and differentiated cells in their response to hypoxia and anoxia/reoxygenation. We conclude that AC16 differentiation leads to proteomic and metabolic shifts and altered cell response to oxygen deprivation. This underscores the requirement for proper selection of particular differentiation state during experimental planning.
    Keywords:  AC16; differentiation; hypoxia; metabolism; mitochondria
    DOI:  https://doi.org/10.1152/ajpcell.00083.2025
  7. Biotechnol J. 2025 Apr;20(4): e70013
      Shake flasks are predominantly used in screening and the early stages of biotechnological process development. However, oxygen-demanding processes cannot easily be performed in shake flasks, since the maximum oxygen transfer capacity is usually smaller than in stirred reactors. Studies during the last decades suggest that the shaking frequency is one of the most crucial cultivation parameters to sustainably increase oxygen supply in orbitally shaken bioreactors. In this study - for the first time - a prototype of a self-balancing orbital shaker was used, which is capable to be operated at up to 750 rpm shaking frequency at 25 mm shaking diameter and 600 rpm at 50 mm. Kluyveromyces lactis cultivations were monitored with a modified TOM system to measure the maximum oxygen transfer capacities (OTRmax) and corresponding kLa values. A maximum kLa value of 650 h-1 (OTRmax = 135 mmol/L/h) was reached at 10 mL filling volume in a 250 mL shake flask made of glass with a hydrophilic surface property. This is an increase of about 50%, compared to current commercial orbital shakers. The new high-speed orbital shaker provides new possibilities for screening applications and process development. High-speed shaking for enhanced oxygen supply is particularly beneficial at 25 mm shaking diameter, rather than at 50 mm, minimizing the impact of the elevated centrifugal force on the shaking system.
    Keywords:  Kluyveromyces lactis; high‐speed shaking; liquid distribution; oxygen transfer rate; shake flask
    DOI:  https://doi.org/10.1002/biot.70013
  8. Am J Physiol Gastrointest Liver Physiol. 2025 Apr 17.
       BACKGROUND: Alcohol-related liver disease (ALD) is one of the leading causes of alcohol-related morbidity and mortality worldwide. Unfortunately, limited therapeutic options are currently available, due to the complex risk factors involved as well as the lack of information on the molecular mechanisms driving its progression. Interestingly, chronic, excessive alcohol intake has been reported to exacerbate the severity of Obstructive sleep apnea (OSA), a respiratory disorder typically characterized by chronic intermittent hypoxia (CIH). However, this relationship between alcohol-enhanced OSA and ALD development/progression remains to be elucidated.
    METHODS: As an approach to investigate this relationship in vivo Gao-binge ALD and CIH mouse models were established. Alcohol-related liver injury, hepatic steatosis, inflammation and oxidative stress were then assessed in these models. In addition, LPS and ethanol-co-treated AML12 hepatocytes served as an in vitro model to investigate the mechanisms through which CIH affects ethanol-induced liver injury.
    RESULTS: CIH intervention ameliorated alcohol-related liver injury, reduced hepatic lipid accumulation and oxidative stress and alleviated liver inflammation. Mechanistically, in the liver of these Gao-binge mice, CIH intervention inhibited alcohol-induced upregulation and activation of hypoxia-inducible factor 2α (HIF-2α), a protein which plays a key role in hepatic lipid metabolism and liver injury. Similar to these effects observed in response to CIH intervention, treatment of Gao-binge mice with the selective inhibitor of HIF-2α, PT2385, alleviated alcohol-related liver injury and steatosis while inhibiting oxidative stress and inflammation. Additional findings from our in vitro model revealed that CIH downregulated HIF-2α by promoting calpains protein expression, thereby reducing the accumulation of lipid droplets and decreasing ROS production in AML12 cells co-challenged with LPS and ethanol.
    CONCLUSIONS: The above results provide important, new evidence that re-conceptualizes the role of alcohol-enhanced OSA in ALD progression. Moreover, these findings can serve as the foundation for the development of HIF-2α inhibitors for use in the prevention and treatment of ALD.
    Keywords:  ALD; Chronic intermittent hypoxia; HIF-2α; Lipid accumulation; ROS
    DOI:  https://doi.org/10.1152/ajpgi.00283.2024
  9. mSystems. 2025 Apr 16. e0134724
      This study investigated alterations in hematological parameters, gut microbiota composition, and fecal and plasma metabolic profiles among high-altitude residents during reoxygenation periods of 1 week, 1 month, and 4 months to elucidate the effects of reoxygenation on human physiology and metabolism. Exposure to high altitudes alters intestinal flora, plasma and fecal metabolites, disrupting their metabolic balance. Distinct differences in amino acid, lipid, energy, immune, cofactor, and vitamin metabolism pathways were detected between high- and low-altitude populations, with a partial recovery of disparities during reoxygenation. Although the gut microbiota exhibited limited adaptive homeostasis to altitude variations, the abundance of microbial taxa and the expression levels of fecal metabolites during the initial reoxygenation phase, particularly during the first week, were sensitive to the reoxygenated environment. Through 16S rRNA gene sequencing and bioinformatics analysis, operational taxonomic units (OTUs) were annotated at the genus level, revealing that the genera Barnesiella, Parabacteroides, and Megasphaera, along with plasma L-arginine, S1P, and alpha-D-glucose, emerged as potential biomarkers for the first week of reoxygenation among high-altitude populations. Notably, a marked change in oxidative stress levels and an increase in antioxidant capacity were observed in high-altitude residents during early reoxygenation. Tyrosine metabolism, which is jointly regulated by the plasma and fecal metabolites and gut microbiota, plays an important role under high-altitude conditions during initial reoxygenation. Additionally, the plasma metabolites pyridoxine and hypoxanthine and the Rothia genus correlated significantly with high-altitude deacclimatization syndrome scores during the first week of reoxygenation.IMPORTANCEOur research focuses on the prompt activation of tyrosine metabolism in plasma following reoxygenation, along with the regulatory mechanisms employed by the intestinal microbiota and the metabolism of feces to modulate this metabolic process. Notably, in the initial stages of reoxygenation, specific microbial genera such as Barnesiella, Parabacteroides, and Megasphaera, alongside plasma biomarkers including L-arginine, S1P, and alpha-D-glucose, emerge as pivotal players. Additionally, our findings reveal a distinct hematological profile characterized by a decrease in the MCHC and increases in the MCV and RDW-SD during the first week of reoxygenation, and this temporal window marked a crucial juncture in the plasma metabolome. Whereas the first month of reoxygenation signified a pivotal phase in the gut microbiome's adaptation to altered environmental conditions, as evidenced by alterations in alpha diversity.
    Keywords:  gut microbiota; hypoxia; metabolism; plateau population; reoxygenation
    DOI:  https://doi.org/10.1128/msystems.01347-24