İklim Değişikliğinin Vektörel Hastalıklara Etkisi ve Kırım Kongo Kanamalı Ateşi Hastalığı

Fatih Dökmedemir; Birgül Piyal

doi:10.20515/otd.1301764

Review

İklim Değişikliğinin Vektörel Hastalıklara Etkisi ve Kırım Kongo Kanamalı Ateşi Hastalığı

Year 2024, Volume: 46 Issue: 2, 317 - 328, 18.03.2024

Fatih Dökmedemir Birgül Piyal

https://doi.org/10.20515/otd.1301764

Abstract

Dünya nüfusunun yarıdan fazlası vektör kaynaklı hastalık riski altındadır. Vektörle bulaşan hastalıklar yüksek ölüm oranı ve yüksek düzeyde engelliliğe neden olmaları nedeniyle halk sağlığını tehdit eden ve ayrıntılı irdelemeyi gerektiren sorunlardır. Küresel sıcaklığın 2100 yılına gelindiğinde ortalama 1 ila 3,5 C⸰ artacağı; ilişkili olarak vektör kaynaklı hastalıkların da daha geniş bir coğrafyada yayılacağı ve prevalansının artacağı öngörülmektedir. Ekolojik değişim Kırım Kongo Kanamalı Ateşinin (KKKA) örüntüsünü etkilemekte ve böylece bulaşma riskini değiştirebilmektedir. İnsandan insana bulaşma potansiyeli düşük olduğu için sadece küçük salgınlar oluşturabilir ancak yüksek ölüm oranları nedeniyle halk sağlığı yönünden üstünde durulması gereken bir hastalıktır. Önleme çalışmalarında ribavirinin yararı kanıtlanmıştır. Tedavide ribavirin etkililiği ise tartışmalıdır. Ayrıca sağlık hizmeti sunumu uygulamaları sürecinde hastalığın bulaş riski yüksektir ve yüksek viral yük nedeniyle büyük olasılıkla ölümle sonuçlanır. Dünya genelinde insan ve hayvan sağlığı ile ilgilenen kuruluşların bu hastalığa karşı koruma ve tedavi yöntemleri geliştirmesi bir halk sağlığı gereksinimidir.

Keywords

İklim Değişikliği, Kırım Kongo Kanamalı Ateşi, Zoonotik Hastalıklar, Sağlık Çalışanları

References

1. Selman M, King TE, Pardo A. American Thoracic Society; European Respiratory Society; American College of Chest Physicians. Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy. Ann. Intern. Med. 2001; 134:136–151
2. Katzen J, Beers MF. Contributions of alveolar epithelial cell quality control to pulmonary fibrosis. J. Clin. Investig. 2020; 130:5088–5099.
3. Kirkwood TB. Understanding the odd science of aging. Cell. 2005; 120: 437–447.
4. Kapetanaki MG, Mora AL, Rojas M. Influence of age on wound healing and fibrosis. J. Pathol. 2013; 229: 310–322.
5. Wynn TA. Integrating mechanisms of pulmonary fibrosis. J. Exp. Med. 2011; 208: 1339–1350.
6. Barkauskas CE, Noble PW. Cellular mechanisms of tissue fibrosis. 7. New insights into the cellular mechanisms of pulmonary fibrosis. Am. J. Physiol. Cell Physiol. 2014; 306: C987–C996.
7. Wynn TA, Ramalingam TR. Mechanisms of fibrosis: Therapeutic translation for fibrotic disease. Nat. Med. 2012; 18: 1028–1040.
8. Hecker L, Logsdon NJ, Kurundkar D, Kurundkar A, Bernard K, Hock T, Meldrum E, Sanders YY, Thannickal VJ. Reversal of persistent fibrosis in aging by targeting Nox4-Nrf2 redox imbalance. Sci. Transl. Med. 2014; 6: 231ra47.
9. Betensley A, Sharif R, Karamichos D. A Systematic Review of the Role of DysfunctionalWound Healing in the Pathogenesis and Treatment of Idiopathic Pulmonary Fibrosis. J. Clin. Med. 2016; 6: 2.
10. Coker RK, Laurent GJ, Shahzeidi S, Lympany PA, du Bois RM, Jeffery PK., McAnulty, RJ. Transforming growth factors-beta (1), -beta (2), and -beta (3) stimulate fibroblast procollagen production in vitro but are differentially expressed during bleomycin-induced lung fibrosis. Am. J. Pathol. 1997; 150: 981–991.
11. Khalil N, O’Connor RN, Unruh HW, Warren PW, Flanders KC, Kemp A, Bereznay OH, Greenberg AH. Increased production and immunohistochemical localization of transforming growth factor-beta in idiopathic pulmonary fibrosis. Am. J. Respir. Cell Mol. Biol. 1991; 5: 155–162.
12. Raghow B, Irish P, Kang AH. Coordinate regulation of transforming growth factor beta gene expression and cell proliferation in hamster lungs undergoing bleomycin-induced pulmonary fibrosis. J. Clin. Investig. 1989; 84: 1836–1842.
13. Heldin CH, Miyazono K, ten Dijke P. TGF-beta signalling from cell membrane to nucleus through SMAD proteins. Nature 1997, 390, 465–471.
14. Zhao J, Shi W, Wang YL, Chen H, Bringas P, Jr., Datto MB, Frederick JP, Wang XF, Warburton D. Smad3 deficiency attenuates bleomycin-induced pulmonary fibrosis in mice. Am. J. Physiol. Lung Cell Mol. Physiol. 2002, 282, L585–L593.
15. Nakao, A.; Afrakhte, M.; Moren, A.; Nakayama, T.; Christian, J.L.; Heuchel, R.; Itoh, S.; Kawabata, M.; Heldin, N.E.; Heldin, C.H.; et al. Identification of Smad7, a TGFbeta-inducible antagonist of TGF-beta signalling. Nature 1997, 389, 631–635.
16. Hayashi H, Abdollah S, Qiu Y, Cai J, Xu YY, Grinnell BW, Richardson MA, Topper JN, Gimbrone MA Jr, Wrana JL et al. The MAD-related protein Smad7 associates with the TGF-beta receptor and functions as an antagonist of TGF-beta signaling. Cell 1997, 89, 1165–1173.
17. Grimminger F, Gunther A, Vancheri C. The role of tyrosine kinases in the pathogenesis of idiopathic pulmonary fibrosis. Eur. Respir. J. 2015, 45, 1426–1433.
18. Antoniades HN, Bravo MA, Avila RE, Galanopoulos T, Neville-Golden J, Maxwell M, Selman M. Platelet-derived growth factor in idiopathic pulmonary fibrosis. J. Clin. Investig. 1990, 86, 1055–1064.
19. Martinet Y, Rom WN, Grotendorst GR, Martin GR, Crystal RG. Exaggerated spontaneous release of platelet-derived growth factor by alveolar macrophages from patients with idiopathic pulmonary fibrosis. N. Engl. J. Med. 1987, 317, 202–209.
20. Liu JY, Morris GF, Lei WH, Hart CE, Lasky JA, Brody AR. Rapid activation of PDGF-A and -B expression at sites of lung injury in asbestos-exposed rats. Am. J. Respir. Cell Mol. Biol. 1997, 17, 129–140.
21. Hoyle GW, Li J, Finkelstein JB, Eisenberg T, Liu JY, Lasky JA, Athas G, Morris GF, Brody AR. Emphysematous lesions, inflammation, and fibrosis in the lungs of transgenic mice overexpressing platelet-derived growth factor. Am. J. Pathol. 1999, 154, 1763–1775.
22. Yi ES, Lee H, Yin S, Piguet P, Sarosi I, Kaufmann S, Tarpley J, Wang NS, Ulich TR. Platelet-derived growth factor causes pulmonary cell proliferation and collagen deposition in vivo. Am. J. Pathol. 1996, 149, 539–548.
23. Yoshida M, Sakuma-Mochizuki J. Abe, K et al. In vivo gene transfer of an extracellular domain of platelet-derived growth factor beta receptor by the HVJ-liposome method ameliorates bleomycin-induced pulmonary fibrosis. Biochem. Biophys. Res. Commun. 1999; 265: 503–508.
24. Rom WN, Basset P, Fells GA, Nukiwa T, et al. Alveolar macrophages release an insulin-like growth factor I-type molecule. J. Clin. Investig. 1988; 82: 1685–1693.
25. Bitterman PB, Adelberg S, Crystal RG. Mechanisms of pulmonary fibrosis. Spontaneous release of the alveolar macrophage-derived growth factor in the interstitial lung disorders. J. Clin. Investig. 1983; 72: 1801–1813.
26. Dees C, M. Tomcik, K. Palumbo-Zerr, et al., Arthritis Rheum, 2012; 64: 3006-3015.
27. Koppikar P, Bhagwat N, Kilpivaara O, Manshouri T, Adli M, Hricik T et al. Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy. Nature. 2012;489(7414):155-9.
28. Dees, C, Chakraborty, D, Distler, JHW. Cellular and molecular mechanisms in fibrosis. Exp. Dermatol.. 2021; 30: 121– 131.
29. Giacomelli C, Piccarducci R, Marchetti L, Romei C, Martini C. Pulmonary Fibrosis from Molecular Mechanisms to Therapeutic Interventions: Lessons from Post-COVID-19 Patients. Biochem. Pharmacol. 2021; 193: 114812.
30. Bartis D, Mise N, Mahida RY, Eickelberg O, Thickett DR. Epithelial–Mesenchymal Transition in Lung Development and Disease: Does It Exist and Is It Important? Thorax. 2014; 69: 760–765.
31. Kim KK, Kugler MC, Wolters PJ, Robillard L, Galvez MG, Brumwell AN, et al. Alveolar Epithelial Cell Mesenchymal Transition Develops in Vivo during Pulmonary Fibrosis and Is Regulated by the Extracellular Matrix. Proc. Natl. Acad. Sci. USA 2006; 103; 13180–13185.
32. Ye Z, Hu Y. TGF-β1: Gentlemanly Orchestrator in Idiopathic Pulmonary Fibrosis (Review). Int. J. Mol. Med. 2021; 48: 132.
33. Akhmetshina A, Palumbo K, Dees C, Bergmann C, Venalis P, et al. Activation of Canonical Wnt Signalling Is Required for TGF-β-Mediated Fibrosis. Nat. Commun. 2012; 3: 735.
34. Zhou B, Liu Y, Kahn M, Ann DK, Han A, Wang H et al. Interactions Between β-Catenin and Transforming Growth Factor-β Signaling Pathways Mediate Epithelial-Mesenchymal Transition and Are Dependent on the Transcriptional Co-Activator CAMP-Response Element-Binding Protein (CREB)-Binding Protein (CBP). J. Biol. Chem. 2012; 287: 7026–7038.
35. Hill C, Li J, Liu D, Conforti F, Brereton CJ, Yao L, et al. Autophagy Inhibition-Mediated Epithelial–Mesenchymal Transition Augments Local Myofibroblast Differentiation in Pulmonary Fibrosis. Cell. Death Dis. 2019; 10: 591.
36. Peng T, Frank DB, Kadzik RS, Morley MP, Rathi KS, Wang T, Zhou S, Cheng L, Lu M.M.; Morrisey EE. Hedgehog Actively Maintains Adult Lung Quiescence and Regulates Repair and Regeneration. Nature 2015, 526, 578–582.
37. Wang C, Cassandras M, Peng T. The Role of Hedgehog Signaling in Adult Lung Regeneration and Maintenance. J. Dev. Biol. 2019, 7, 14.
38. Bolaños AL, Milla CM, Lira JC, Ramírez R, Checa M, Barrera L, García-Alvarez J, Carbajal V, Becerril C, Gaxiola M. et al. Role of Sonic Hedgehog in Idiopathic Pulmonary Fibrosis. Am. J. Physiol. Lung Cell. Mol. Physiol. 2012, 303, L978–L990.
39. Fitch PM, Howie SEM, Wallace WAH. Oxidative Damage and TGF-β Differentially Induce Lung Epithelial Cell Sonic Hedgehog and Tenascin-C Expression: Implications for the Regulation of Lung Remodelling in Idiopathic Interstitial Lung Disease: SHH and Tenascin-C in Type-II Alveolar Cells. Int. J. Exp. Pathol. 2011, 92, 8–17.
40. Stewart GA, Hoyne GF, Ahmad SA, Jarman E, Wallace WA, Harrison DJ, Haslett C, Lamb JR, Howie SE. Expression of the Developmental Sonic Hedgehog (Shh) Signalling Pathway Is up-Regulated in Chronic Lung Fibrosis and the Shh Receptor Patched 1 Is Present in Circulating T Lymphocytes. J. Pathol. 2003, 199, 488–495.
41. Henke C, Marineili W, Jessurun J, Fox J, Harms D, Peterson M, Chiang L, Doran P. Macrophage production of basic fibroblast growth factor in the fibroproliferative disorder of alveolar fibrosis after lung injury. Am. J. Pathol. 1993, 143, 1189–1199.
42. Inoue Y, King TE, Jr., Tinkle SS, Dockstader K, Newman LS. Human mast cell basic fibroblast growth factor in pulmonary fibrotic disorders. Am. J. Pathol. 1996; 149: 2037–2054.
43. Romero Y, Bueno M, Ramirez R, Álvarez D, Sembrat JC, Goncharova EA, et al. MTORC1 Activation Decreases Autophagy in Aging and Idiopathic Pulmonary Fibrosis and Contributes to Apoptosis Resistance in IPF Fibroblasts. Aging Cell 2016; 15: 1103–1112.
44. Wang Y, Huang G, Wang Z, Qin H, Mo B, Wang, C. Elongation Factor-2 Kinase Acts Downstream of P38 MAPK to Regulate Proliferation, Apoptosis and Autophagy in Human Lung Fibroblasts. Exp. Cell. Res. 2018; 363: 291–298.
45. Ogawa T, Shichino S, Ueha S, Matsushima K. Macrophages in Lung Fibrosis. Int. Immunol. 2021; 33: 665–671.
46. Phan THG, Paliogiannis P, Nasrallah GK, Giordo R, Eid AH et al. Emerging Cellular and Molecular Determinants of Idiopathic Pulmonary Fibrosis. Cell. Mol. Life Sci. 2021; 78: 2031–2057.
47. Heukels P, Moor CC, von der Thüsen JH, Wijsenbeek MS, Kool M. Inflammation and Immunity in IPF Pathogenesis and Treatment. Respir. Med. 2019; 147: 79–91.

The Effect of Climate Change on Vectorial Diseases and Crimean-Congo Hemorrhagic Fever

Year 2024, Volume: 46 Issue: 2, 317 - 328, 18.03.2024

Fatih Dökmedemir Birgül Piyal

https://doi.org/10.20515/otd.1301764

Abstract

More than half of the world's population is at risk of vector-borne diseases. Vector-borne diseases are problems that threaten public health and require detailed investigation due to their high mortality rate and high level of disability. Global temperature will increase by 1 to 3.5 C⸰ on average by 2100; In relation to this, it is predicted that vector-borne diseases will spread in a wider geography and their prevalence will increase. Ecological change affects the pattern of Crimean-Congo Hemorrhagic Fever and thus can change the risk of transmission. Since it has a low human-to-human transmission potential, it can only cause small epidemics, but it is a disease that should be considered in terms of public health due to its high mortality rates. The benefit of ribavirin has been proven in prevention studies. The efficacy of ribavirin in treatment is controversial. In addition, the risk of transmission of the disease is high in the process of health care delivery practices and it is likely to result in death due to high viral load. It is a public health requirement that organizations dealing with human and animal health around the world develop protection and treatment methods against this disease.

Keywords

Climate Change, Crimean-Congo Hemorrhagic Fever, Zoonotic Diseases, Health Workers

References

1. Selman M, King TE, Pardo A. American Thoracic Society; European Respiratory Society; American College of Chest Physicians. Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy. Ann. Intern. Med. 2001; 134:136–151
2. Katzen J, Beers MF. Contributions of alveolar epithelial cell quality control to pulmonary fibrosis. J. Clin. Investig. 2020; 130:5088–5099.
3. Kirkwood TB. Understanding the odd science of aging. Cell. 2005; 120: 437–447.
4. Kapetanaki MG, Mora AL, Rojas M. Influence of age on wound healing and fibrosis. J. Pathol. 2013; 229: 310–322.
5. Wynn TA. Integrating mechanisms of pulmonary fibrosis. J. Exp. Med. 2011; 208: 1339–1350.
6. Barkauskas CE, Noble PW. Cellular mechanisms of tissue fibrosis. 7. New insights into the cellular mechanisms of pulmonary fibrosis. Am. J. Physiol. Cell Physiol. 2014; 306: C987–C996.
7. Wynn TA, Ramalingam TR. Mechanisms of fibrosis: Therapeutic translation for fibrotic disease. Nat. Med. 2012; 18: 1028–1040.
8. Hecker L, Logsdon NJ, Kurundkar D, Kurundkar A, Bernard K, Hock T, Meldrum E, Sanders YY, Thannickal VJ. Reversal of persistent fibrosis in aging by targeting Nox4-Nrf2 redox imbalance. Sci. Transl. Med. 2014; 6: 231ra47.
9. Betensley A, Sharif R, Karamichos D. A Systematic Review of the Role of DysfunctionalWound Healing in the Pathogenesis and Treatment of Idiopathic Pulmonary Fibrosis. J. Clin. Med. 2016; 6: 2.
10. Coker RK, Laurent GJ, Shahzeidi S, Lympany PA, du Bois RM, Jeffery PK., McAnulty, RJ. Transforming growth factors-beta (1), -beta (2), and -beta (3) stimulate fibroblast procollagen production in vitro but are differentially expressed during bleomycin-induced lung fibrosis. Am. J. Pathol. 1997; 150: 981–991.
11. Khalil N, O’Connor RN, Unruh HW, Warren PW, Flanders KC, Kemp A, Bereznay OH, Greenberg AH. Increased production and immunohistochemical localization of transforming growth factor-beta in idiopathic pulmonary fibrosis. Am. J. Respir. Cell Mol. Biol. 1991; 5: 155–162.
12. Raghow B, Irish P, Kang AH. Coordinate regulation of transforming growth factor beta gene expression and cell proliferation in hamster lungs undergoing bleomycin-induced pulmonary fibrosis. J. Clin. Investig. 1989; 84: 1836–1842.
13. Heldin CH, Miyazono K, ten Dijke P. TGF-beta signalling from cell membrane to nucleus through SMAD proteins. Nature 1997, 390, 465–471.
14. Zhao J, Shi W, Wang YL, Chen H, Bringas P, Jr., Datto MB, Frederick JP, Wang XF, Warburton D. Smad3 deficiency attenuates bleomycin-induced pulmonary fibrosis in mice. Am. J. Physiol. Lung Cell Mol. Physiol. 2002, 282, L585–L593.
15. Nakao, A.; Afrakhte, M.; Moren, A.; Nakayama, T.; Christian, J.L.; Heuchel, R.; Itoh, S.; Kawabata, M.; Heldin, N.E.; Heldin, C.H.; et al. Identification of Smad7, a TGFbeta-inducible antagonist of TGF-beta signalling. Nature 1997, 389, 631–635.
16. Hayashi H, Abdollah S, Qiu Y, Cai J, Xu YY, Grinnell BW, Richardson MA, Topper JN, Gimbrone MA Jr, Wrana JL et al. The MAD-related protein Smad7 associates with the TGF-beta receptor and functions as an antagonist of TGF-beta signaling. Cell 1997, 89, 1165–1173.
17. Grimminger F, Gunther A, Vancheri C. The role of tyrosine kinases in the pathogenesis of idiopathic pulmonary fibrosis. Eur. Respir. J. 2015, 45, 1426–1433.
18. Antoniades HN, Bravo MA, Avila RE, Galanopoulos T, Neville-Golden J, Maxwell M, Selman M. Platelet-derived growth factor in idiopathic pulmonary fibrosis. J. Clin. Investig. 1990, 86, 1055–1064.
19. Martinet Y, Rom WN, Grotendorst GR, Martin GR, Crystal RG. Exaggerated spontaneous release of platelet-derived growth factor by alveolar macrophages from patients with idiopathic pulmonary fibrosis. N. Engl. J. Med. 1987, 317, 202–209.
20. Liu JY, Morris GF, Lei WH, Hart CE, Lasky JA, Brody AR. Rapid activation of PDGF-A and -B expression at sites of lung injury in asbestos-exposed rats. Am. J. Respir. Cell Mol. Biol. 1997, 17, 129–140.
21. Hoyle GW, Li J, Finkelstein JB, Eisenberg T, Liu JY, Lasky JA, Athas G, Morris GF, Brody AR. Emphysematous lesions, inflammation, and fibrosis in the lungs of transgenic mice overexpressing platelet-derived growth factor. Am. J. Pathol. 1999, 154, 1763–1775.
22. Yi ES, Lee H, Yin S, Piguet P, Sarosi I, Kaufmann S, Tarpley J, Wang NS, Ulich TR. Platelet-derived growth factor causes pulmonary cell proliferation and collagen deposition in vivo. Am. J. Pathol. 1996, 149, 539–548.
23. Yoshida M, Sakuma-Mochizuki J. Abe, K et al. In vivo gene transfer of an extracellular domain of platelet-derived growth factor beta receptor by the HVJ-liposome method ameliorates bleomycin-induced pulmonary fibrosis. Biochem. Biophys. Res. Commun. 1999; 265: 503–508.
24. Rom WN, Basset P, Fells GA, Nukiwa T, et al. Alveolar macrophages release an insulin-like growth factor I-type molecule. J. Clin. Investig. 1988; 82: 1685–1693.
25. Bitterman PB, Adelberg S, Crystal RG. Mechanisms of pulmonary fibrosis. Spontaneous release of the alveolar macrophage-derived growth factor in the interstitial lung disorders. J. Clin. Investig. 1983; 72: 1801–1813.
26. Dees C, M. Tomcik, K. Palumbo-Zerr, et al., Arthritis Rheum, 2012; 64: 3006-3015.
27. Koppikar P, Bhagwat N, Kilpivaara O, Manshouri T, Adli M, Hricik T et al. Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy. Nature. 2012;489(7414):155-9.
28. Dees, C, Chakraborty, D, Distler, JHW. Cellular and molecular mechanisms in fibrosis. Exp. Dermatol.. 2021; 30: 121– 131.
29. Giacomelli C, Piccarducci R, Marchetti L, Romei C, Martini C. Pulmonary Fibrosis from Molecular Mechanisms to Therapeutic Interventions: Lessons from Post-COVID-19 Patients. Biochem. Pharmacol. 2021; 193: 114812.
30. Bartis D, Mise N, Mahida RY, Eickelberg O, Thickett DR. Epithelial–Mesenchymal Transition in Lung Development and Disease: Does It Exist and Is It Important? Thorax. 2014; 69: 760–765.
31. Kim KK, Kugler MC, Wolters PJ, Robillard L, Galvez MG, Brumwell AN, et al. Alveolar Epithelial Cell Mesenchymal Transition Develops in Vivo during Pulmonary Fibrosis and Is Regulated by the Extracellular Matrix. Proc. Natl. Acad. Sci. USA 2006; 103; 13180–13185.
32. Ye Z, Hu Y. TGF-β1: Gentlemanly Orchestrator in Idiopathic Pulmonary Fibrosis (Review). Int. J. Mol. Med. 2021; 48: 132.
33. Akhmetshina A, Palumbo K, Dees C, Bergmann C, Venalis P, et al. Activation of Canonical Wnt Signalling Is Required for TGF-β-Mediated Fibrosis. Nat. Commun. 2012; 3: 735.
34. Zhou B, Liu Y, Kahn M, Ann DK, Han A, Wang H et al. Interactions Between β-Catenin and Transforming Growth Factor-β Signaling Pathways Mediate Epithelial-Mesenchymal Transition and Are Dependent on the Transcriptional Co-Activator CAMP-Response Element-Binding Protein (CREB)-Binding Protein (CBP). J. Biol. Chem. 2012; 287: 7026–7038.
35. Hill C, Li J, Liu D, Conforti F, Brereton CJ, Yao L, et al. Autophagy Inhibition-Mediated Epithelial–Mesenchymal Transition Augments Local Myofibroblast Differentiation in Pulmonary Fibrosis. Cell. Death Dis. 2019; 10: 591.
36. Peng T, Frank DB, Kadzik RS, Morley MP, Rathi KS, Wang T, Zhou S, Cheng L, Lu M.M.; Morrisey EE. Hedgehog Actively Maintains Adult Lung Quiescence and Regulates Repair and Regeneration. Nature 2015, 526, 578–582.
37. Wang C, Cassandras M, Peng T. The Role of Hedgehog Signaling in Adult Lung Regeneration and Maintenance. J. Dev. Biol. 2019, 7, 14.
38. Bolaños AL, Milla CM, Lira JC, Ramírez R, Checa M, Barrera L, García-Alvarez J, Carbajal V, Becerril C, Gaxiola M. et al. Role of Sonic Hedgehog in Idiopathic Pulmonary Fibrosis. Am. J. Physiol. Lung Cell. Mol. Physiol. 2012, 303, L978–L990.
39. Fitch PM, Howie SEM, Wallace WAH. Oxidative Damage and TGF-β Differentially Induce Lung Epithelial Cell Sonic Hedgehog and Tenascin-C Expression: Implications for the Regulation of Lung Remodelling in Idiopathic Interstitial Lung Disease: SHH and Tenascin-C in Type-II Alveolar Cells. Int. J. Exp. Pathol. 2011, 92, 8–17.
40. Stewart GA, Hoyne GF, Ahmad SA, Jarman E, Wallace WA, Harrison DJ, Haslett C, Lamb JR, Howie SE. Expression of the Developmental Sonic Hedgehog (Shh) Signalling Pathway Is up-Regulated in Chronic Lung Fibrosis and the Shh Receptor Patched 1 Is Present in Circulating T Lymphocytes. J. Pathol. 2003, 199, 488–495.
41. Henke C, Marineili W, Jessurun J, Fox J, Harms D, Peterson M, Chiang L, Doran P. Macrophage production of basic fibroblast growth factor in the fibroproliferative disorder of alveolar fibrosis after lung injury. Am. J. Pathol. 1993, 143, 1189–1199.
42. Inoue Y, King TE, Jr., Tinkle SS, Dockstader K, Newman LS. Human mast cell basic fibroblast growth factor in pulmonary fibrotic disorders. Am. J. Pathol. 1996; 149: 2037–2054.
43. Romero Y, Bueno M, Ramirez R, Álvarez D, Sembrat JC, Goncharova EA, et al. MTORC1 Activation Decreases Autophagy in Aging and Idiopathic Pulmonary Fibrosis and Contributes to Apoptosis Resistance in IPF Fibroblasts. Aging Cell 2016; 15: 1103–1112.
44. Wang Y, Huang G, Wang Z, Qin H, Mo B, Wang, C. Elongation Factor-2 Kinase Acts Downstream of P38 MAPK to Regulate Proliferation, Apoptosis and Autophagy in Human Lung Fibroblasts. Exp. Cell. Res. 2018; 363: 291–298.
45. Ogawa T, Shichino S, Ueha S, Matsushima K. Macrophages in Lung Fibrosis. Int. Immunol. 2021; 33: 665–671.
46. Phan THG, Paliogiannis P, Nasrallah GK, Giordo R, Eid AH et al. Emerging Cellular and Molecular Determinants of Idiopathic Pulmonary Fibrosis. Cell. Mol. Life Sci. 2021; 78: 2031–2057.
47. Heukels P, Moor CC, von der Thüsen JH, Wijsenbeek MS, Kool M. Inflammation and Immunity in IPF Pathogenesis and Treatment. Respir. Med. 2019; 147: 79–91.

There are 47 citations in total.

Details

Primary Language	Turkish
Subjects	Health Care Administration
Journal Section	DERLEME
Authors	Fatih Dökmedemir 0000-0001-8998-8585 Birgül Piyal 0000-0003-4170-0444
Publication Date	March 18, 2024
Published in Issue	Year 2024 Volume: 46 Issue: 2

Cite

Vancouver	Dökmedemir F, Piyal B. İklim Değişikliğinin Vektörel Hastalıklara Etkisi ve Kırım Kongo Kanamalı Ateşi Hastalığı. Osmangazi Tıp Dergisi. 2024;46(2):317-28.

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