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LUNG FIBROSIS IN COVID-19 SURVIVORS: HISTONE DEACETYLASE INHIBITORS AS A PROMISING THERAPEUTIC STRATEGY

DOI: https://doi.org/10.29296/25877313-2021-08-01
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Issue: 
8
Year: 
2021

K.A. Aitbaev Dr.Sc. (Med.), Professor, Head of the Department of Head. Laboratory of Pathological Physiology, Board Member of Chronic Kidney Disease Specialists Society of Kyrgyzstan; (Bishkek, Kyrgyzstan) ORCID:0000-0003-4973-039X E-mail: kaitbaev@yahoo.com I.T. Murkamilov Ph.D. (Med.), Acting Associate Professor of the Department of Faculty Therapy of Kyrgyz State Medical Academy named after I.K. Akhunbaev; Senior Lecturer, Kyrgyz-Russian Slavic University, Nephrologist, Chairman of the Board of Chronic Kidney Disease Specialists Society of Kyrgyzstan (Bishkek, Kyrgyzstan) ORCID:0000-0001-8513-9279 E-mail: murkamilov.i@mail.ru Zh.A. Murkamilova Post-graduate Student, the Department of Therapy № 2, SEI HPE Kyrgyz-Russian Slavic University (Bishkek, Kyrgyzstan) ORCID:0000-0002-7653-0433 E-mail:murkamilovazh.t@mail.ru V.V. Fomin Dr.Sc. (Med.), Professor, Corresponding Member of RAS, Head of the Department of Faculty Therapy № 1, Sklifosovsky Institute; Vice-rector in Clinical Work and Continuous Professional Education, I.M. Sechenov First Moscow State Medical University (Sechenov University) of the Ministry of Healthcare of Russia (Moscow, Russia) ORCID: 0000-0002-2682-4417 E-mail: fomin@mma.ru I.O. Kudaibergenova Dr.Sc. (Med.), Professor, Rector of the Kyrgyz State Medical Academy named after I.K. Akhunbaev (Bishkek, Kyrgyzstan) ORCID: 0000-0003-3007-8127 E-mail: k_i_o2403@mail.ru F.A. Yusupov Dr.Sc. (Med.), Professor, Head of the Department Neurology, Psychiatry and Neurosurgery of Medicinal Faculty of Osh State University; Board Member of Chronic Kidney Disease Specialists Society of Kyrgyzstan; Chief Neurologist of Southern Region of Kyrgyzstan (Osh, Kyrgyzstan) ORCID: 0000-0003-0632-6653 Е-mail: furcat_y@mail.ru

Over the past twenty years, the world has witnessed several viral epidemics such as the Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), influenza A subtype H1N1 virus, Middle East Respiratory Syndrome Coronavirus (MERS-CoV), and more recently the novel SARS-CoV coronavirus 2, which caused the disease COVID-19. The latest epidemic proved to be the most destructive and claimed more than 2 million lives. Today's efforts to combat COVID-19 are focused on controlling the spread of the coronavirus and identifying effective treatment options. Meanwhile, an analysis of data regarding the long-term clinical consequences of previous coronavirus infections (SARS-CoV and MERS-CoV) shows that with the removal of the virus from the body, the pathological process in many cases does not end and can develop into long-term lung damage, in particular, fibrous interstitial disease or pulmonary fibrosis. Thus, pulmonary fibrosis can become an ongoing problem in patients recovering from COVID-19. Therefore, it is necessary now to determine the strategy of preventive measures both to counteract the development of pulmonary fibrosis in patients with COVID-19 during inpatient treatment, and to prevent its occurrence and progression in the long term. Although anti-fibrotic drugs such as pirfenidone and nintedanib have been shown to be effective in reducing the rate of deterioration in lung function, their results have not significantly improved patient recovery. In addition, the use of these drugs has been associated with serious side effects. In this regard, the purpose of this article is to consider the use of histone deacety-lase inhibitors (HDACs) as an alternative epigenetic therapy strategy to prevent the development or progression of pulmonary fibrosis in recovered SARS-CoV-2 patients

Keywords: 
COVID-19
SARS-CoV-2
pulmonary fibrosis
TGF-β
HDAC inhibitors
epigenetics

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References: 
  1. Wang H., Li X., Li T., et al. The genetic sequence, origin, and diag-nosis of SARS- CoV-2. Eur. J. Clin. Microbiol. Infect. Dis. Off Publ. Eur. Soc. Clin. Microbiol. 2020; https://doi.org/10.1007/s10096-020-03899-4
  2. CDC, Coronavirus disease 2019 (COVID-19), in: Cent. Dis. Con-trol Prev, 2020. https://www.cdc.gov/coronavirus/2019-ncov/need-extra-precautions/evidence-table.html. (Accessed 25 July 2020).
  3. Gu J., Korteweg C. Pathology and pathogenesis of severe acute respiratory syndrome. Am. J. Pathol 2007; 170:1136–1147. https://doi.org/10.2353/ ajpath.2007.061088
  4. Zhang P., Li J., Liu H., et al. Long-term bone and lung conse-quences associated with hospital-acquired severe acute respiratory syndrome: a 15-year follow-up from a prospective cohort study. Bone Res. 2020; 8: 8. https://doi.org/10.1038/ s41413-020-0084-5
  5. Tse G.M., To K.F., Chan P.K., et al. Pulmonary pathological fea-tures in coronavirus associated severe acute respiratory syndrome (SARS). J. Clin. Pathol. 2004; 57: 260–265. https://doi.org/10.1136/jcp.2003.013276
  6. Antonio G.E., Wong K.T., Hui D.S., et al. Thin-section CT in pa-tients with severe acute respiratory syndrome following hospital discharge: preliminary experience. Radiology. 2003; 228: 810–815. https://doi.org/10.1148/radiol.2283030726
  7. Wong K.T., Antonio G.E., Hui D.S., et al. Severe acute respiratory syndrome: thin- section computed tomography features, temporal changes, and clinicoradiologic correlation during the convalescent period. J. Comput. Assist. Tomogr. 2004; 28: 790–795. https://doi.org/10.1097/00004728-200411000-00010
  8. Wu X., Dong D., Ma D. Thin-section computed tomography manifestations during convalescence and long-term follow-up of patients with severe acute respiratory syndrome (SARS). Med. Sci. Monit. Int. Med. J. Exp.Clin. Res. 2016; 22: 2793–2799. https://doi.org/10.12659/msm.896985
  9. Müller N.L., Ooi G.C., Khong P.L., et al. High-resolution CT find-ings of severe acute respiratory syndrome at presentation and after admission. AJR Am. J. Roentgenol. 2004; 182:
  10. 39–44. https://doi.org/10.2214/ajr.182.1.1820039
  11. Chu W.C., Li A.M., Ng A.W., et al. Thin-section CT 12 months after the diagnosis of severe acute respiratory syndrome in pediatric pa-tients. AJR Am. J. Roentgenol. 2006; 186: 1707–1714. https://doi.org/10.2214/AJR.05.0382
  12. Das K.M., Lee E.Y., Singh R., et al. Follow-up chest radiographic findings in patients with MERS-CoV after recovery. Indian J. Ra-diol. Imaging. 2017; 27: 342–349. https://doi.org/10.4103/ijri.IJRI_469_16
  13. Mossel E.C., Wang J., Jeffers S., et al. SARS-CoV replicates in primary human alveolar type II cell cultures but not in type I-like cells. Virology. 2008; 372: 127–135. https://doi.org/10.1016/j.virol.2007.09.045
  14. Weinheimer V.K., Becher A., Tönnies M., et al. Influenza A viruses target type II pneumocytes in the human lung. J. Infect. Dis. 2012; 206: 1685–1694. https://doi. org/10.1093/infdis/jis455
  15. Delpino M.V., Quarleri J. SARS-CoV-2 pathogenesis: imbalance in the renin- angiotensin system favors lung fibrosis. Front. Cell. Infect. Microbiol. 2020; 10: 340. https://doi.org/10.3389/fcimb.2020.00340
  16. Kogan E.A., Berezovskij Ju.S., Protsenko D.D. i dr. Patologi-cheskaja anatomija infektsii, vyzvannoj SARS-CoV-2. Sudebnaja meditsina. 2020; 6(2): 8–30. https://doi.org/ 10.19048/2411-8729-2020-6-2-8-30 (Kogan E.A., Berezovsky Yu.S, Protsenko D.D., et al. Pathological Anatomy of Infection Caused by SARS-CoV-2. Russian Journal of Forensic Medicine. 2020; 6(2): 8–30. https://doi.org/ 10.19048/2411-8729-2020-6-2-8-30 (in Russian)].
  17. Ni W., Yang X., Yang D., et al. Role of angiotensin-converting en-zyme 2 (ACE2) in COVID-19. Crit Care Lond Engl. 2020; 24: 422. https://doi.org/10.1186/s13054- 020-03120-0
  18. Leng L., Cao R., Ma J., et al. Pathological features of COVID-19-associated lung injury: a preliminary proteomics report based on clinical samples. Signal Transduct Target Ther. 2020; 5: 240. https://doi.org/10.1038/s41392-020-00355-9
  19. Meyer K.C. Pulmonary fibrosis, part I: epidemiology, pathogenesis, and diagnosis. Expert Rev Respir Med. 2017; 11: 343–359. https://doi.org/10.1080/ 17476348.2017.1312346
  20. Richeldi L., Collard H.R., Jones M.J. Idiopathic pulmonary fibro-sis. Lancet Lond Engl. 2017 389: 1941–1952. https://doi.org/10.1016/S0140-6736(17)30866-8
  21. Vallʹee A., Lecarpentier Y. TGF-β in fibrosis by acting as a conductor for contractile properties of myofibroblasts. Cell Biosci. 2019; 9: 98. https://doi.org/10.1186/ s13578-019-0362-3
  22. Wynn T.A. Cellular and molecular mechanisms of fibrosis. J. Pathol. 2008;214:199–210. https://doi.org/10.1002/path.2277
  23. Pardo A., Cabrera S., Maldonado M., Selman M. Role of matrix metalloproteinases in the pathogenesis of idiopathic pulmonary fibrosis. Respir. Res. 2016; 17: 23. https://doi.org/10.1186/s12931-016-0343-6
  24. George P.M., Wells A.U., Jenkins R.G. Pulmonary fibrosis and COVID-19: the potential role for antifibrotic therapy. Lancet Respir. Med. 2020; https://doi.org/ 10.1016/S2213-2600(20)30225-3
  25. Leask A. COVID-19: is fibrosis the killer? J. Cell. Commun. Sig-nal. 2020; 14: 255. https://doi.org/10.1007/s12079-020-00569-0
  26. Wu C., Chen X., Cai Y., et al. Risk factors associated with acute respiratory distress syndrome and death in patients with corona-virus disease 2019 pneumonia in Wuhan, China. JAMA Intern. Med. 2020; https://doi.org/10.1001/ jamainternmed.2020.0994
  27. Yu M., Liu Y., Xu D., et al. Prediction of the development of pulmo-nary fibrosis using serial thin-section CT and clinical features in pa-tients discharged after treatment for COVID-19 pneumonia. Korean J. Radiol. 2020; 21: 746–755. https://doi.org/10.3348/kjr.2020.0215
  28. MGH FLARE. June 2 - will COVID-19 cause more IPF? https://us19.campaign-archive.com/?u=ef98149bee3f299584374540a&id=737fad9de0. (Accessed 28 November 2020).
  29. Ojo A.S., Balogun S.A., Williams O.T., Ojo O.S. Pulmonary fibro-sis in COVID-19 survivors: predictive factors and risk reduction strategies. Pulm Med. 2020;2020:6175964. https://doi.org/10.1155/2020/6175964
  30. Wigén J., Löfdahl A., Bjermer L., et al. Converging pathways in pulmonary fibrosis and Covid-19 - the fibrotic link to disease se-verity. Respir Med X. 2 2020; 100023. https://doi.org/10.1016/j.yrmex.2020.100023
  31. Kobayashi T., Tanaka K., Fujita T., et al. Bidirectional role of IL-6 signal in pathogenesis of lung fibrosis. Respir. Res. 2015; 16: 99. https://doi.org/10.1186/ s12931-015-0261-z
  32. Pustovetova M.G., Chikinev Ju.A., Piontkovskaja K.A. Mole-kuljarno-kletochnye mehanizmy razvitija fibroza legkih i spontannogo pnevmotoraksa. Bjulleten' SO RAMN. 2014; 34(5): 17-21 [Pustovetova M.G., Chikinev Yu.A., Piontkovskaya K.A. Molecular cell mechanisms of development of pulmonary fi-brosis and spontaneous pneumothorax. Bulletin of the SB RAMS 2014; 34(5): 17-21 (in Russian)].
  33. Minshall E.M., Leung D.Y., Martin R.J., et al. Eosinophil-associated TGF-beta1 mRNA expression and airways fibrosis in bronchial asthma. Am. J. Respir. Cell Mol. Biol. 1997; 17: 326–333. https://doi.org/10.1165/ajrcmb.17.3.2733
  34. Khalil N., O’Connor R.N., Flanders K.C., et al. TGF-beta 1, but not TGF-beta 2 or TGF-beta 3, is differentially present in epithelial cells of advanced pulmonary fibrosis: an immunohistochemical study. Am. J. Respir. Cell Mol. Biol. 1996; 14:131–138. https://doi.org/10.1165/ajrcmb.14.2.8630262
  35. Khalil N., Parekh T.V., O’Connor R., et al. Regulation of the ef-fects of TGF-beta 1 by activation of latent TGF-beta 1 and differen-tial expression of TGF-beta receptors (T beta R-I and T beta R-II) in idiopathic pulmonary fibrosis. Thorax. 2001; 56:907–915. https://doi.org/10.1136/thorax.56.12.907
  36. Roberts A.B., Piek E., Böttinger E.P., et al. Is Smad3 a major player in signal transduction pathways leading to fibrogenesis? Chest. 2001; 120: 43S–47S. https:// doi.10.1378/chest.120.1_suppl.s43-a
  37. Leask A., Abraham D.J. TGF-beta signaling and the fibrotic re-sponse. FASEB J. Off. Publ. Fed. Am. Soc. Exp. Biol. 2004; 18:816–827. https://doi.org/10.1096/fj.03-1273rev
  38. Kandasamy M., Lehner B., Kraus S., et al. TGF-beta signalling in the adult neurogenic niche promotes stem cell quiescence as well as generation of new neurons. J. Cell. Mol. Med. 2014; 18: 1444–1459. https://doi.org/10.1111/ jcmm.12298
  39. Venkataraman T., Frieman M.B. The role of epidermal growth fac-tor receptor (EGFR) signaling in SARS coronavirus-induced pul-monary fibrosis. Antivir. Res. 2017; 143: 142–150. https://doi.org/10.1016/j.antiviral.2017.03.022
  40. Watanabe-Takano H., Takano K., Hatano M., et al. DA-Raf-mediated suppression of the Ras-ERK pathway is essential for TGF-β1-induced epithelial-mesenchymal transition in alveolar epi-thelial type 2 cells. PLoS One. 2015; 10:e0127888. https://doi.org/10.1371/journal.pone.0127888
  41. Zhao X., Nicholls J.M., Chen Y.G. Severe acute respiratory syn-drome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-beta signaling. J. Biol. Chem. 2008; 283: 3272–3280. https://doi.org/10.1074/jbc.M708033200
  42. Allen J.T., Knight R.A., Bloor C.A., et al. Enhanced insulin-like growth factor binding protein-related protein 2 (connective tissue growth factor) expression in patients with idiopathic pulmonary fi-brosis and pulmonary sarcoidosis. Am. J. Respir. Cell Mol. Biol. 1999; 21: 693–700. https://doi.org/ 10.1165/ajrcmb.21.6.3719
  43. Torr E.E., Ngam C.R., Bernau K., et al. Myofibroblasts exhibit en-hanced fibronectin assembly that is intrinsic to their contractile phe-notype. J. Biol. Chem. 2015; 290: 6951–6961. https://doi.org/10.1074/jbc.M114.606186
  44. Desmouliʹere A., Geinoz A., Gabbiani F., et al. Transforming growth factor- beta 1 induces alpha-smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts. J. Cell Biol. 1993; 122: 103–111. https://doi.org/10.1083/jcb.122.1.103
  45. Rajasekaran S., Vaz M., Reddy S.P. Fra-1/AP-1 transcription factor negatively regulates pulmonary fibrosis in vivo. PLoS One. 2012; 7:e41611. https://doi.org/ 10.1371/journal.pone. 0041611
  46. Shi K., Jiang J., Ma T., et al. Pathogenesis pathways of idiopathic pulmonary fibrosis in bleomycin-induced lung injury model in mice. Respir. Physiol. Neurobiol. 2014; 190: 113–117. https://doi.org/10.1016/j.resp.2013.09.011
  47. Pattarayan D., Rajarajan D., Ayyanar S., et al. C-phycocyanin suppresses transforming growth factor-β1-induced epithelial mes-enchymal transition in human epithelial cells. Pharmacol Rep PR. 2017; 69: 426–431. https://doi.org/ 10.1016/j.pharep.2016.12.013
  48. Pattarayan D., Thimmulappa R.K., Ravikumar V., Rajasekaran S. Diagnostic potential of extracellular microRNA in respiratory diseases. Clin. Rev. Allergy Immunol. 2018; 54: 480–492. https://doi.org/10.1007/s12016-016-8589-9
  49. Rajasekaran S., Rajaguru P., Sudhakar Gandhi P.S. MicroRNAs as potential targets for progressive pulmonary fibrosis. Front. Pharmacol. 2015; 6: 254. https://doi. org/10.3389/fphar.2015.00254
  50. Myllärniemi M., Kaarteenaho R. Pharmacological treatment of idiopathic pulmonary fibrosis - preclinical and clinical studies of pirfenidone, nintedanib, and N-acetylcysteine. EurClinRespir J. 2015; 2. https://doi.org/10.3402/ecrj. v2.26385
  51. Margaritopoulos G.A., Vasarmidi E., Antoniou K.M. Pirfenidone in the treatment of idiopathic pulmonary fibrosis: an evidence-based review of its place in therapy. Core Evid 2016; 11: 11–22. https://doi.org/10.2147/CE.S76549
  52. Kato M., Sasaki S., Nakamura T., et al. Gastrointestinal adverse ef-fects of nintedanib and the associated risk factors in patients with idiopathic pulmonary fibrosis. Sci. Rep. 2019; 9: 12062. https://doi.org/10.1038/s41598-019-48593-4
  53. Zhang H. A Randomized Open-label Study to Evaluate the Efficacy and Safety of Pirfenidone in Patients With Severe and Critical Novel Coronavirus Infection. Slinic. altrials. Gov. 2020.
  54. Pleasants R., Tighe R.M. Management of idiopathic pulmonary fi-brosis. Ann. Pharmacother. 2019; 53: 1238–1248. https://doi.org/10.1177/ 1060028019862497
  55. Tang J., Yan H., Zhuang S. Histone deacetylases as targets for treatment of multiple diseases. Clin. Sci (Lond.). 2013 jun; 124(11): 651–662. https://doi.org/1042/CS20120504
  56. Glenisson W., Castronovo V., Waltregny D. Histone deacetylase 4 is required for TGFbeta1-induced myofibroblastic differentiation. Biochim. Biophys. Acta. 2007; 1773: 1572–1582. https://doi.org/10.1016/j.bbamcr.2007.05.016
  57. Guo W., Shan B., Klingsberg R.C., et al. Abrogation of TGF-beta1-induced fibroblast-myofibroblast differentiation by histone deacety-lase inhibition. Am. J. Physiol. Lung. Cell. Mol. Physiol. 2009; 297: L864–L870. https://doi.org/10.1152/ ajplung.00128.2009
  58. Korfei M., Skwarna S., Henneke I., et al. Aberrant expression and activity of histone deacetylases in sporadic idiopathic pulmonary fi-brosis. Thorax. 2015; 70: 1022–1032. https://doi.org/10.1136/thoraxjnl-2014-206411
  59. Barter M.J., Pybus L., Litherland G.J., et al. HDAC-mediated con-trol of ERK- and PI3K-dependent TGF-β-induced extracellular ma-trix-regulating genes. Matrix. Biol. J. Int. Soc. Matrixju Biol. 2010; 29: 602–612. https://doi.org/10.1016/j. matbio.2010.05.002
  60. Jones D.L., Haak A.J., Caporarello N., et al. TGFβ-induced fibro-blast activation requires persistent and targeted HDAC-mediated gene repression. J. Cell Sci. 2019; 132. https://doi.org/10.1242/jcs.233486
  61. Saito S., Zhuang Y., Suzuki T., et al. HDAC8 inhibition ameliorates pulmonary fibrosis. Am. J. Physiol. Lung. Cell. Mol. Physiol. 2019; 316: L175–L186. https://doi. org/10.1152/ajplung.00551.2017
  62. Yoon S., Kang G., Eom G.H. HDAC inhibitors: therapeutic poten-tial in fibrosis-associated human diseases. Int. J. Mol. Sci. 2019; 20. https://doi.org/10.3390/ ijms20061329
  63. Coward W.R., Watts K., Feghali-Bostwick C.A., et al. Defective histone acetylation is responsible for the diminished expression of cyclooxygenase 2 in idiopathic pulmonary fibrosis. Mol. Cell. Biol. 2009; 29: 4325–4339. https://doi.org/ 10.1128/MCB.01776-08
  64. Huang S.K., Scruggs A.M., Donaghy J., et al. Histone modifica-tions are responsible for decreased Fas expression and apoptosis resistance in fibrotic lung fibroblasts. Cell. Death Dis. 2013;4:e621. https://doi.org/10.1038/cddis.2013.146
  65. Saito S., Zhuang Y., Shan B., et al. Tubastatin ameliorates pulmo-nary fibrosis by targeting the TGFβ-PI3K-Akt pathway. PLoS One. 2017; 12:e0186615. https://doi. org/10.1371/ journal.pone.0186615
  66. Korfei M., Stelmaszek D., MacKenzie B., et al. Comparison of the antifibrotic effects of the pan-histone deacetylase-inhibitor pano-binostat versus the IPF-drug pirfenidone in fibroblasts from pa-tients with idiopathic pulmonary fibrosis. PLoS One. 2018; 13:e0207915. https://doi.org/10.1371/journal. pone.0207915