China
Africa
Explore chapters and articles related to this topic
Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
Moving back to the biology. Knowing what we now know from the above, we might ask ourselves: How does hypoxia increase erythropoiesis to increase the haematocrit, and what is the role of HIF-1 and erythropoietin (EPO)? French researchers first showed that hypoxia increases erythrocyte numbers and suggested that a hormone, later termed erythropoietin, might be responsible for the increased erythropoiesis in response to hypoxia (14). A dissection study then identified the kidney as the main source of systemic EPO synthesis (15), with liver also contributing, but to a lesser extent (16).
Alternative Tumor-Targeting Strategies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Studies have also shown that a heterodimeric transcription factor, Hypoxia Inducible Factor-1 (HIF-1), plays an important role in allowing tumor cells to adapt to a hypoxic environment. On detecting hypoxic conditions, HIF-1, which normally resides in the cytoplasm of cells, dimerizes and translocates to the nucleus where it binds to its cognate sequence in the promoter regions of key genes, and stimulates the expression of proteins that help the cell cope in its new harsher environment. Some of these expressed genes also lead to resistance to certain families of anticancer agents.
History of high altitude medicine and physiology
Published in Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson, Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson
As will become apparent in subsequent chapters in this book, one of the burgeoning areas of hypoxia research in recent years has been the role of the hypoxia-inducible factor (HIF). The pathway mediated by this gene transcription factor, which was discovered and worked out by William Kaelin Jr, Sir Peter Ratcliffe, and Gregg Semenza (Figure 1.13), is active in every cell and controls hundreds of downstream genes and physiologic processes in animals and humans. Further detailed information can be found in subsequent chapters of this book and several recent reviews (Ivan and Kaelin 2017; Schödel and Ratcliffe 2019; Semenza 2014). The work by these and other investigators has provided researchers and clinicians new routes for treatment of anemia, cancer, heart disease, and many other conditions and, in the years to come, is likely to fundamentally transform our understanding of most topics explored in this book. In recognition of the significance of this work, Kaelin, Ratcliffe, and Semenza were awarded the Nobel Prize in Physiology or Medicine in 2019.
Recent advances in targeted drug delivery for the treatment of pancreatic ductal adenocarcinoma
Published in Expert Opinion on Drug Delivery, 2022
The dense stroma not only creates a physical barrier to drug delivery but also prevents the diffusion of oxygen within the solid tumor. In addition, due to unrestricted cell growth, the increased oxygen demand further aggravates the degree of hypoxia within the tumor[45]. When a hypoxic environment develops, hypoxia-inducible factors (HIF) mediate the adaptive physiological response of tumor cells to hypoxia[46]. HIF is involved in multiple malignant progressions of cancer, including cell stemness, metabolic reprogramming, autocrine growth factor signaling, epithelial-mesenchymal transition, tumor invasion, metastasis, and resistance to radiotherapy and chemotherapy[42,47–49]. Hypoxia may also lead to immunosuppression, and it has been shown that HIF induces the recruitment of myeloid-derived suppressor cells (MDSC) as well as regulatory T cells (Treg), and result in apoptosis of T cells, making the tumor tolerant to immunotherapy[50,51].
Effect of ghrelin on hypoxia-related cardiac angiogenesis: involvement of miR-210 signalling pathway
Published in Archives of Physiology and Biochemistry, 2022
Fariba Mirzaei Bavil, Elham Karimi-Sales, Alireza Alihemmati, Mohammad Reza Alipour
In the present study, hypoxia exposure stimulated myocardial angiogenesis which was accompanied by higher protein expression levels of HIF-1α and VEGF. In this regard, it has been documented that hypoxia stimulates the expression of a group of genes, which are responsible for hypoxia-adaptive responses by activation of HIF-1 (Gupta et al.2018). Therefore, HIF-1 is the master regulator of angiogenesis during hypoxic conditions (Zimna and Kurpisz 2015). In agreement with the present study, an early study suggested that hypoxia acts as a strong inducer of VEGF expression and therefore, increases cardiac capillary cell growth (Ladoux and Frelin 1993). Moreover, consistent with this study, previous studies have suggested that hypoxia acts as a driving force for tumour angiogenesis, which is mainly accomplished by the HIF-1α-mediated up-regulation of VEGF (Shweiki et al.1992, Zagzag et al.2000, Pugh and Ratcliffe 2003).
The Expression and Role of Hypoxia-induced Factor-1α in Human Tenon’s Capsule Fibroblasts under Hypoxia
Published in Current Eye Research, 2021
Xi Qin, Keling Wu, Chengguo Zuo, Mingkai Lin
We first detected VEGF in HTFs, since it is a major response factor to HIF-1α. Activation of the VEGF gene is triggered during hypoxia by increased HIF-1α accumulation as a compensatory mechanism aimed at stimulating angiogenesis and thus increasing oxygen delivery.20 Our results were consistent with this finding. In our work, VEGF increased with increasing HIF-1α. It has been suggested that VEGF is upregulated in the aqueous humor of glaucoma patients and in the rabbit model and stimulates fibroblast proliferation in vitro; inhibition of VEGF reduces scar formation after GFS.21 On the other hand, HIF-1α was overexpressed in aging mice, and skin neovascularization can be seen.22 Therefore, it might be useful to regulate wound healing after GFS by regulating HIF-1α, which is upstream of VEGF.