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2021, Número 2

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Sal Jal 2021; 8 (2)


La hipoxia y la infl amación en el desarrollo de las enfermedades crónico-degenerativas

Mazorra-Carrillo JL, Barbero-Becerra VJ, Esquivel-Solís H
Texto completo Cómo citar este artículo Artículos similares

Idioma: Español
Referencias bibliográficas: 64
Paginas: 104-112
Archivo PDF: 290.98 Kb.


PALABRAS CLAVE

Hipoxia, inflamación, HIF-1, enfermedades crónicas.

RESUMEN

Las enfermedades crónicas son las primeras causas de discapacidad y mortalidad en todo el mundo. Estas enfermedades cursan con inflamación e hipoxia persistentes. La hipoxia consiste en una disminución del oxígeno intracelular que provoca la activación del factor inducible por hipoxia HIF-1α y en el núcleo de las células induce la expresión de genes involucrados en angiogénesis, eritropoyesis, metabolismo, supervivencia e inflamación. Esta relación recíproca entre la hipoxia y la inflamación conduce a la disfunción y la degeneración tisular, características de las enfermedades crónicas. En esta revisión destacamos los aspectos relevantes sobre los cambios moleculares inducidos por la hipoxia y HIF-1 α en la expresión génica y su implicación en la patogenia de las enfermedades crónico-degenerativas.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Nature S. 2020 Springer Nature Limited.

  2. Pahwa R, Jialal I. Chronic infl ammation. 2019.

  3. Amarante-Mendes GP, Adjemian S, Branco LM, Zanetti LC, Weinlich R, Bortoluci KR. Pattern Recognition Receptors and the Host Cell Death Molecular Machinery. Front Immunol . 2018;9:2379. https://www.frontiersin.org/article/10.3389/ fi mmu.2018.02379.

  4. Żeromski J, Kaczmarek M, Boruczkowski M, Kierepa A, Kowala-Piaskowska A, Mozer-Lisewska I. Signifi cance and Role of Pattern Recognition Receptors in Malignancy. Arch Immunol Th er Exp (Warsz). 2019;67(3):133-141. doi:10.1007/s00005- 019-00540-x.

  5. Liu T, Zhang L, Joo D, Sun S-C. NF-κB signaling in infl ammation. Signal Transduct Target Th er. 2017;2(1):17023. doi:10.1038/ sigtrans.2017.23.

  6. Sun S-C. Th e non-canonical NF-κB pathway in immunity and infl ammation. Nat Rev Immunol. 2017;17(9):545-558. doi:10.1038/nri.2017.52.

  7. Naik R. Exam Preparatory Manual for Undergraduates: General & Systemic Pathology. 2015.

  8. Sugimoto MA, Sousa LP, Pinho V, Perretti M, Teixeira MM. Resolution of Infl ammation: What Controls Its Onset?. Front Immunol. 2016;7:160. https://www.frontiersin.org/ article/10.3389/fi mmu.2016.00160.

  9. Organization WH. Th e top 10 causes of death World Health Organization. 2017.

  10. Biddlestone J, Bandarra D, Rocha S. Th e role of hypoxia in infl ammatory disease (review). Int J Mol Med. 2015;35(4):859- 869. doi:10.3892/ijmm.2015.2079.

  11. Barrett KE, Barman SM, Brooks HL, Yuan JX-J. Ganong’s Review of Medical Physiology. McGraw-Hill Education; 2019.

  12. Hsia CCW, Schmitz A, Lambertz M, Perry SF, Maina JN. Evolution of air breathing: oxygen homeostasis and the transitions from water to land and sky. Compr Physiol. 2013;3(2):849-915.

  13. Tortora GJ, Derrickson BH. Principles of Anatomy and Physiology. John Wiley & Sons; 2018.

  14. Salehi E, Eft ekhari R, Oraei M, Gharib A, Bidad K. MicroRNAs in rheumatoid arthritis. Clin Rheumatol. 2015;34(4):615-628.

  15. Jeff ery RC. Clinical features of rheumatoid arthritis. Medicine (Baltimore). 2010;38(4):167-171.

  16. Özenci V, Kouwenhoven M, Link H. Cytokines in multiple sclerosis: methodological aspects and pathogenic implications. Mult Scler J. 2002;8(5):396-404.

  17. Imitola J, Chitnis T, Khoury SJ. Cytokines in multiple sclerosis: from bench to bedside. Pharmacol Th er. 2005;106(2):163-177.

  18. Hasheminia SJ, Tolouei S, ZARKESH ESH, et al. Cytokine gene expression in newly diagnosed multiple sclerosis patients. 2015.

  19. Pellicoro A, Ramachandran P, Iredale JP, Fallowfi eld J a. Liver fi brosis and repair: immune regulation of wound healing in a solid organ. Nat Rev Immunol. 2014;14(3):181-194. doi:10.1038/ nri3623.

  20. Czaja AJ. Hepatic infl ammation and progressive liver fi brosis in chronic liver disease. World J Gastroenterol. 2014;20(10):2515- 2532. doi:10.3748/wjg.v20.i10.2515.

  21. Ortega LM, Fornoni A. Role of cytokines in the pathogenesis of acute and chronic kidney disease, glomerulonephritis, and end-stage kidney disease. Int J Interf Cytokine Mediat Res. 2010;2(1):49-62.

  22. Levey AS, Coresh J. Chronic kidney disease Lancet (Vol. 379, pp. 165-180). 2012.

  23. Chung KF. Cytokines in chronic obstructive pulmonary disease. Eur Respir J. 2001;18(34 suppl):50s - 59s.

  24. Eickmeier O, Huebner M, Herrmann E, et al. Sputum biomarker profi les in cystic fi brosis (CF) and chronic obstructive pulmonary disease (COPD) and association between pulmonary function. Cytokine. 2010;50(2):152-157.

  25. Calverley PMA, Georgopoulos D. Chronic obstructive pulmonary disease: symptoms and signs. Eur Respir Monogr. 2006;38:7.

  26. Davies JC, Alton EWFW, Bush A. Cystic fi brosis. BMJ. 2007;335(7632):1255 LP - 1259. doi:10.1136/bmj.39391.713229.AD.

  27. Ramachandran A. Know the signs and symptoms of diabetes. Indian J Med Res. 2014;140(5):579.

  28. King GL. Th e role of infl ammatory cytokines in diabetes and its complications. J Periodontol. 2008;79:1527-1534.

  29. Ramani G V, Uber PA, Mehra MR. Chronic heart failure: contemporary diagnosis and management. In: Mayo Clinic Proceedings. Vol 85. Elsevier; 2010:180-195.

  30. Kaptoge S, Seshasai SRK, Gao P, et al. Infl ammatory cytokines and risk of coronary heart disease: new prospective study and updated meta-analysis. Eur Heart J. 2014;35(9):578-589.

  31. Nanduri J, Yuan G, Kumar GK, Semenza GL, Prabhakar NR. Transcriptional responses to intermittent hypoxia. Respir Physiol Neurobiol. 2008;164(1-2):277-281. doi:10.1016/j. resp.2008.07.006.

  32. Semenza GL, Wang GL. A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation. Mol Cell Biol. 1992;12(12):5447-5454. doi:10.1128/mcb.12.12.5447.

  33. Hu C-J, Wang L-Y, Chodosh LA, Keith B, Simon MC. Diff erential roles of hypoxia-inducible factor 1α (HIF-1α) and HIF-2α in hypoxic gene regulation. Mol Cell Biol. 2003;23(24):9361-9374.

  34. Kaelin Jr WG, Ratcliff e PJ. Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway. Mol Cell. 2008;30(4):393-402.

  35. Zimna A, Kurpisz M. Hypoxia-inducible factor-1 in physiological and pathophysiological angiogenesis: applications and therapies. Biomed Res Int. 2015;2015.

  36. Semenza GL. Hydroxylation of HIF-1: oxygen sensing at the molecular level. Physiology. 2004;19(4):176-182.

  37. Brune B, Zhou J. Th e role of nitric oxide (NO) in stability regulation of hypoxia inducible factor-1α (HIF-1α). Curr Med Chem. 2003;10(10):845-855.

  38. Tanaka H, Yamamoto M, Hashimoto N, et al. Hypoxiaindependent overexpression of hypoxia-inducible factor 1α as an early change in mouse hepatocarcinogenesis. Cancer Res. 2006;66(23):11263-11270.

  39. Nishi K, Oda T, Takabuchi S, et al. LPS induces hypoxia-inducible factor 1 activation in macrophage-diff erentiated cells in a reactive oxygen species–dependent manner. Antioxid Redox Signal. 2008;10(5):983-996.

  40. Carreau A, Hafny-rahbi B El, Matejuk A, Grillon C, Kieda C. Why is the partial oxygen pressure of human tissues a crucial parameter ? Small molecules and hypoxia Imaging of hypoxic areas. 2011;15(6):1239-1253. doi:10.1111/j.1582-4934.2011.01258.x.

  41. Eltzschig HK, Carmeliet P. Hypoxia and infl ammation. N Engl J Med. 2011;364(7):656-665.

  42. Ziello JE, Jovin IS, Huang Y. Hypoxia-Inducible Factor (HIF)-1 regulatory pathway and its potential for therapeutic intervention in malignancy and ischemia. Yale J Biol Med. 2007;80(2):51.

  43. Eltzschig HK. Targeting Hypoxia-induced Infl ammation. Anesthesiology. 2011;114(2):239-242. doi:10.1097/ ALN.0b013e3182070c66.

  44. Cramer T, Yamanishi Y, Clausen BE, et al. HIF-1α is essential for myeloid cell-mediated infl ammation. Cell. 2003;112(5):645-657.

  45. Dweik RA. Nitric oxide, hypoxia, and superoxide: the good, the bad, and the ugly! 2005.

  46. Deng W, Feng X, Li X, Wang D, Sun L. Hypoxia-inducible factor 1 in autoimmune diseases. Cell Immunol. 2016;303:7-15.

  47. Jiang F, Tang Y-T, Guo L, Jiao X. Th e role of insulin-like growth factor I and hypoxia inducible factor 1α in vascular endothelial growth factor expression in type 2 diabetes. Ann Clin Lab Sci. 2013;43(1):37-44.

  48. Pichu S, Sathiyamoorthy J, Krishnamoorthy E, Umapathy D, Viswanathan V. Impact of the hypoxia inducible factor-1α (HIF- 1α) pro582ser polymorphism and its gene expression on diabetic foot ulcers. Diabetes Res Clin Pract. 2015;109(3):533-540.

  49. Gu HF, Zheng X, Seman NA, et al. Impact of the hypoxiainducible factor-1 α (HIF1A) Pro582Ser polymorphism on diabetes nephropathy. Diabetes Care. 2013;36(2):415-421.

  50. Al-Shukaili AK, Al-Jabri AA. Rheumatoid arthritis, cytokines and hypoxia. Saudi Med J. 2006;27(11):1642-1649.

  51. Li G, Zhang Y, Qian Y, et al. Interleukin-17A promotes rheumatoid arthritis synoviocytes migration and invasion under hypoxia by increasing MMP2 and MMP9 expression through NF-κB/HIF-1α pathway. Mol Immunol. 2013;53(3):227-236.

  52. Hu F, Mu R, Zhu J, et al. Hypoxia and hypoxia-inducible factor- 1α provoke toll-like receptor signalling-induced infl ammation in rheumatoid arthritis. Ann Rheum Dis. 2014;73(5):928-936.

  53. Hu F, Liu H, Xu L, et al. Hypoxia‐inducible factor‐1α perpetuates synovial fi broblast interactions with T cells and B cells in rheumatoid arthritis. Eur J Immunol. 2016;46(3):742-751.

  54. Park SY, Lee SW, Kim HY, Lee WS, Hong KW, Kim CD. HMGB1 induces angiogenesis in rheumatoid arthritis via HIF‐1α activation. Eur J Immunol. 2015;45(4):1216-1227.

  55. Ju C, Colgan SP, Eltzschig HK. Hypoxia-inducible factors as molecular targets for liver diseases. J Mol Med. 2016;94(6):613- 627.

  56. Suzuki T, Shinjo S, Arai T, Kanai M, Goda N. Hypoxia and fatty liver. World J Gastroenterol WJG. 2014;20(41):15087.

  57. Aron-Wisnewsky J, Minville C, Tordjman J, et al. Chronic intermittent hypoxia is a major trigger for non-alcoholic fatty liver disease in morbid obese. J Hepatol. 2012;56(1):225-233.

  58. Arias-Loste MT, Fábrega E, López-Hoyos M, Crespo J. Th e crosstalk between hypoxia and innate immunity in the development of obesity-related nonalcoholic fatty liver disease. Biomed Res Int. 2015;2015.

  59. Nath B, Levin I, Csak T, et al. Hepatocyte‐specifi c hypoxiainducible factor‐1α is a determinant of lipid accumulation and liver injury in alcohol‐induced steatosis in mice. Hepatology. 2011;53(5):1526-1537.

  60. Moczydlowska J, Miltyk W, Hermanowicz A, Lebensztejn DM, Palka JA, Debek W. HIF-1 α as a key factor in bile duct ligationinduced liver fi brosis in rats. J Investig Surg. 2017;30(1):41-46.

  61. Copple BL, Kaska S, Wentling C. Hypoxia-inducible factor activation in myeloid cells contributes to the development of liver fi brosis in cholestatic mice. J Pharmacol Exp Th er. 2012;341(2):307-316.

  62. Lolmede K, de Saint Front VD, Galitzky J, Lafontan M, Bouloumie A. Eff ects of hypoxia on the expression of proangiogenic factors in diff erentiated 3T3-F442A adipocytes. Int J Obes. 2003;27(10):1187.

  63. He Q, Gao Z, Yin J, Zhang J, Yun Z, Ye J. Regulation of HIF- 1α activity in adipose tissue by obesity-associated factors: adipogenesis, insulin, and hypoxia. Am J Physiol Metab. 2011;300(5):E877-E885.

  64. Lee YS, Kim J, Osborne O, et al. Increased adipocyte O2 consumption triggers HIF-1α, causing infl ammation and insulin resistance in obesity. Cell. 2014;157(6):1339-1352.




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