Oxygen, carried mainly by erythrocytes, plays a crucial role in human organisms--as the terminal electron acceptor enables mitochondria functioning and energy production. Oxygen excess may be a cause of the damage of basic structural organism components--proteins, lipids and nucleinic acids. Thus, from the biological point of view, regulation of oxygen supply with its detection mechanisms is a critical process. Erythrocyte content optima-lization, in means of "benefit-loss" is a compromise between the necessity of anaerobic metabolism transit (in case of too low erythrocyte count), excessive increase in blood viscosity and non-productive, increased red blood cell turn-over with increased erythrocyte level. It is in fact a process of adaptation to changeable environmental conditions, life style and possible pathological processes. The study is a review of knowledge on the oxygen sensor and its connection to erythropoiesis regulation.
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Eur J Breast Health
January 2025
Department of General Surgery, Elazığ Fethi Sekin City Hospital, University of Health Sciences Turkey, Elazığ, Turkey.
Objective: Triple negative breast carcinoma (TNBC) is characterized by the absence of estrogen receptor, progesterone receptor and human epidermal growth factor receptor-2 receptor expression. Carbonic anhydrase IX (CA IX) is a tumor-associated cell surface glycoprotein that is involved in adaptation to hypoxia-induced acidosis and plays a role in cancer progression. The aim of this study was to investigate CA IX expression in TNBC and its relationship with treatment effect.
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December 2024
Department of Horticulture and Crop Science, The Ohio State University, Columbus, OH, United States.
Field pennycress () is a new biofuel winter annual crop with extreme cold hardiness and a short life cycle, enabling off-season integration into corn and soybean rotations across the U.S. Midwest.
View Article and Find Full Text PDFInt J Med Sci
January 2025
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
This study investigates the role of Fundc1 in cardiac protection under high-altitude hypoxic conditions and elucidates its underlying molecular mechanisms. Using cardiomyocyte-specific knockout ( ) mice, we demonstrated that deficiency exacerbates cardiac dysfunction under simulated high-altitude hypoxia, manifesting as impaired systolic and diastolic function. Mechanistically, we identified that Fundc1 regulates cardiac function through the mitochondrial unfolded protein response (mito-UPR) pathway.
View Article and Find Full Text PDFCrit Rev Clin Lab Sci
January 2025
Institute of Metabolism and Systems Research (IMSR), University of Birmingham, Birmingham, West Midlands, UK.
We present a series of three articles on the genetics and pharmacogenetics of G protein- coupled receptors (GPCR). In the first article, we discuss genetic variants of the G protein subunits and accessory proteins that are associated with human phenotypes; in the second article, we build upon this to discuss "G protein-coupled receptor (GPCR) gene variants and human genetic disease" and in the third article, we survey "G protein-coupled receptor pharmacogenomics". In the present article, we review the processes of ligand binding, GPCR activation, inactivation, and receptor trafficking to the membrane in the context of human genetic disease resulting from pathogenic variants of accessory proteins and G proteins.
View Article and Find Full Text PDFJ Inflamm Res
December 2024
Department of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Rheumatoid arthritis (RA) is an inflammatory autoimmune disease, primarily characterized by chronic symmetric synovial inflammation and erosive bone destruction.Mitochondria, the primary site of cellular energy production, play a crucial role in energy metabolism and possess homeostatic regulation capabilities. Mitochondrial function influences the differentiation, activation, and survival of both immune and non-immune cells involved in RA pathogenesis.
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