[1] Palmer B F, Clegg D J. Oxygen sensing and metabolic homeostasis[J]. Molecular and Cellular Endocrinology, 2014, 397(1-2):51-58.
[2] Wilkins S E, Abboud M I, Hancock R L, et al. Targeting protein-protein interactions in the HIF system[J]. Current Medicinal Chemistry, 2016, 11(8):773-786.
[3] Mevissen T E T, Komander D. Mechanisms of deubiquitinase specificity and regulation[J]. Annual Review of Biochemistry, 2017, 86:159-192.
[4] Wiesener M S, Jurgensen J S, Rosenberger C, et al. Widespread hypoxia-inducible expression of HIF-2alpha in distinct cell populations of different organs[J]. The FASEB Journal, 2003, 17(2):271-273.
[5] Heidbreder M, Frohlich F, Johren O, et al. Hypoxia rapidly activates HIF-3alpha mRNA expression[J]. The FASEB Journal, 2003, 17(11):1541-1543.
[6] Fong G H, Takeda K. Role and regulation of prolyl hydroxylase domain proteins[J]. Cell Death and Differentiation, 2008, 15(4):635-641.
[7] Liu Q, Davidoff O, Niss K, et al. Hypoxia-inducible factor regulates hepcidin via erythropoietin-induced erythropoiesis[J]. Journal of Clinical Investigation, 2012, 122(12):4635-4644.
[8] Drevytska T, Gavenauskas B, Drozdovska S, et al. HIF-3alpha mRNA expression changes in different tissues and their role in adaptation to intermittent hypoxia and physical exercise[J]. Pathophysiology, 2012, 19(3):205-214.
[9] Tojo Y, Sekine H, Hirano I, et al. Hypoxia signaling cascade for erythropoietin production in hepatocytes[J]. Molecular and Cellular Endocrinology, 2015, 35(15):2658-2672.
[10] Biggar P, Kim G H. Treatment of renal anemia:Erythropoiesis stimulating agents and beyond[J]. Kidney Research and Clinical Practice Abbreviation, 2017, 36(3):209-223.
[11] Ashby D R, Gale D P, Busbridge M, et al. Plasma hepcidin levels are elevated but responsive to erythropoietin therapy in renal disease[J]. Kidney International, 2009, 75(9):976-981.
[12] Gupta N, Wish J B. Hypoxia-inducible factor prolyl hydroxylase inhibitors:A potential new treatment for anemia in patients with CKD[J]. American Journal of Kidney Diseases, 2017, 69(6):815-826.
[13] Zhong H, Zhou T, Li H, et al. The role of hypoxia-inducible factor stabilizers in the treatment of anemia in patients with chronic kidney disease[J]. Drug Design Development and Therapy, 2018, 12:3003-3011.
[14] Drueke T B, Parfrey P S. Summary of the KDIGO guideline on anemia and comment:Reading between the (guide)line(s)[J]. Kidney International, 2012, 82(9):952-960.
[15] Cizman B, Sykes A P, Paul G, et al. An exploratory study of daprodustat in erythropoietin-hyporesponsive subjects[J]. Kidney International Report, 2018, 3(4):841-850.
[16] Pezzuto A, Carico E. Role of HIF-1 in cancer progression:Novel insights. A review[J]. Current Molecular Medicine, 2018, 18(6):343-351.
[17] Balamurugan K. HIF-1 at the crossroads of hypoxia, inflammation, and cancer[J]. International Journal of Cancer, 2016, 138(5):1058-1066.
[18] Cho H, Kaelin W G. Targeting HIF2 in clear cell renal cell carcinoma[J]. Cold Spring Harbor Symposia on Quantitative Biology, 2016, 81:113-121.
[19] Wigerup C, Pahlman S, Bexell D. Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer[J]. Pharmacology & Therapeutics, 2016, 164:152-169.
[20] Duan C. Hypoxia-inducible factor 3 biology:Complexities and emerging themes[J]. American Journal of Physiology, 2016, 310(4):C260-269.
[21] Yu T, Tang B, Sun X. Development of inhibitors targeting hypoxia-inducible factor 1 and 2 for cancer therapy[J]. Yonsei Medical Journal, 2017, 58(3):489-496.
[22] Miranda E, Nordgren I K, Male A L, et al. A cyclic peptide inhibitor of HIF-1 heterodimerization that inhibits hypoxia signaling in cancer cells[J]. Journal of the American Chemical Society, 2013, 135(28):10418-10425.
[23] Lee S H, Wolf P L, Escudero R, et al. Early expression of angiogenesis factors in acute myocardial ischemia and infarction[J]. New England Journal of Medicine, 2000, 342(9):626-633.
[24] Kido M, Du L, Sullivan C C, et al. Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse[J]. Journal of the American College of Cardiology, 2005, 46(11):2116-2124.
[25] Huang Y, Hickey R P, Yeh J L, et al. Cardiac myocytespecific HIF-1alpha deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart[J]. The FASEB Journal, 2004, 18(10):1138-1140.
[26] Jain T, Nikolopoulou E A, Xu Q, et al. Hypoxia inducible factor as a therapeutic target for atherosclerosis[J]. Pharmacology & Therapeutics, 2018, 183:22-33.
[27] Christoph M, Ibrahim K, Hesse K, et al. Local inhibition of hypoxia-inducible factor reduces neointima formation after arterial injury in ApoE-/-mice[J]. Atherosclerosis, 2014, 233(2):641-647.
[28] Palazon A, Goldrath A W, Nizet V, et al. HIF transcription factors, inflammation, and immunity[J]. Immunity, 2014, 41(4):518-528.
[29] Taylor C T, Colgan S P. Regulation of immunity and inflammation by hypoxia in immunological niches[J]. Nature Reviews Immunology, 2017, 17(12):774-785.
[30] Ma C, Wei J, Zhan F, et al. Urinary hypoxia-inducible factor-1alpha levels are associated with histologic chronicity changes and renal function in patients with lupus nephritis[J]. Yonsei Medical Journal, 2012, 53(3):587-592.
[31] Hu F, Shi L, Mu R, et al. Hypoxia-inducible factor-1alpha and interleukin 33 form a regulatory circuit to perpetuate the inflammation in rheumatoid arthritis[J]. PLoS One, 2013, 8(8):e72650.
[32] Marik C, Felts P A, Bauer J, et al. Lesion genesis in a subset of patients with multiple sclerosis:a role for innate immunity[J]. Brain, 2007, 130(Pt 11):2800-2815.
[33] Hu F, Liu H, Xu L, et al. Hypoxia-inducible factor-1alpha perpetuates synovial fibroblast interactions with T cells and B cells in rheumatoid arthritis[J]. European Journal of Immunology, 2016, 46(3):742-751.
[34] Barteczek P, Li L, Ernst A S, et al. Neuronal HIF-1alpha and HIF-2alpha deficiency improves neuronal survival and sensorimotor function in the early acute phase after ischemic stroke[J]. Journal of Cerebral Blood Flow & Metabolism, 2017, 37(1):291-306.
[35] Li C, Zhang B, Zhu Y, et al. Post-stroke constraint-induced movement therapy increases functional recovery, angiogenesis, and neurogenesis with enhanced expression of HIF-1alpha and VEGF[J]. Current Neurovascular Research, 2017, 14(4):368-377.