Document Type : Review Article

Author

Dept. Of Surgery, Monash University, Melbourne, Australia

10.7508/ijp.2015.02.001

Abstract

Fibrosis is the pathological condition resulting in the growth of excess fibrous connective tissue in an organ or body system as a reparative or reactive process. In the field of clinical pathology, clinicians and medical scientists are endeavoring to translate experimental knowledge into effective, innovative treatments for a range of fibrotic conditions. The amelioration of whole organ function is at the forefront of research involving new treatment modalities. The augmentation of cardiac function following myocardial infarction is one area of research currentlyundergoing rapid growth internationally, but pulmonary and hepatic functions are both affected by fibrosis in numerous disease states, and chronic allograft fibrosis is an increasingly recognized problem in organ transplantation; novel treatments are thus undergoing development with ever increasing urgency. An attempt will be made to explore the dynamics of fibrosis in a range of disease states not classically recognized as having a common etiology.

Keywords

  1. Puvaneswary M, Joshua F, Ratnarajah S. Idiopathic hypereosinophilic syndrome: magnetic resonance imaging findings in endomyocardial fibrosis. Australas Radiol 2001; 45(4):524-7.
  2. Niino T, Shiono M, Yamamoto T. A case of left ventricular  endomyocardial  fibrosis.  Ann  Thorac Cardiovasc Surg 2002; 8(3):173-6.
  3. Chopra P, Narula J, Talwar KK. Histomorphologic characteristics of endomyocardial fibrosis: an endomyocardial biopsy study. Hum Pathol 1990; 21(6):613-6.
  4. Mousseaux E, Hernigou A, Azencot M. Endomyocardial fibrosis: electron-beam CT features. Radiology 1996; 198(3):755-60.
  5. Zabsonre P, Renambot J, Adoh-Adoh M. Conduction disorders in chronic parietal endocarditis or endomyocardial fibrosis: 170 cases at the Cardiology Institute of Abidjan. Dakar Med 2000; 45(1):15-9.
  6. Nadrous HF, Pellikka PA, Krowka MJ. Pulmonary hypertension in patients with idiopathic pulmonary fibrosis. Chest 2005;128(4):2393-9.
  7. Lettieri CJ, Nathan SD, Barnett S, Ahmad S, Shorr AF. Prevalence and outcomes of pulmonary arterial hypertension  in  idiopathic  pulmonary  fibrosis.  Chest 2006;129(3):746-52.
  8. Honma  K,  Chiyotani  K.  Diffuse  interstitial  fibrosis in non-asbestos pneumoconiosis: a pathological study. Respiration 1993;60(2):120-6.
  9. Hunninghake G, Lynch DA, Galvin JR. Radiologic  findings  are  strongly  associated  with  a  pathologic diagnosis of usual interstitial pneumonia. Chest 2003;124(4):1215-23..
  10. Martinez FJ, Safrin S, Weycker D. The clinical course  of  patients  with  idiopathic  pulmonary  fibrosis. Ann Intern Med 2005;142(12):963-7.
  11. Raghu G. Idiopathic pulmonary fibrosis: treatment options in pursuit of evidence-based approaches. Eur Respir J 2006;28(3):463-5.
  12. Kudo H, Nakayama K, Yanai M. Anticoagulant  therapy  for  idiopathic  pulmonary  fibrosis.  Chest 2005;128(3):1475-82.
  13. Solic N, Wilson J, Wilson SJ, Shute JK. Endothelial activation and increased heparan sulfate expression  in  cystic  fibrosis.  Am  J  Respir  Crit  Care  Med 2005;172(7):892–8.
  14. Harris JF, Fischer MJ, Hotchkiss JR, Monia BP, Randell SH, Harkema JR, et al.Bcl-2 sustains increased mucous and epithelial cell numbers in metaplastic airway epithelium. Am J Respir Crit Care Med 2005;171(7):764–772.
  15. Katabami M, Dosaka-Akita, K Honma, K Kimura, M Fujino, Y Uchida, et al.p53 and Bcl-2 expression in pneumoconiosis-related precancerous lesions and lung cancers: frequent and preferential p53 expression in pneumoconiotic bronchiolar dysplasias. IntJ Cancer 1998;75(4): 504-11 .
  16. Black D, Bird MA, Samson CM, Lyman S, Lange PA, Schrum LW, et al.Primary cirrhotic hepatocytes resist TGFbeta-induced apoptosis through a ROSdependent mechanism. J Hepatol 2004;40(6): 942  -51.
  17. O’Grady JG. Liver transplantation alcohol related liver disease: stirring a hornet’s nest. Gut 2006;55(11):1529-31 .
  18. Benyon RC, Arthur MJP. Extracellular matrix degradation and the role of hepatic stellate cells. Semin Liver Dis 2001;21(3):373-84.
  19. Canbay A, Feldstein A, Baskin-Bey E, Bronk SF, Gores GJ. The caspase inhibitor IDN-6556 attenuates hepatic injury and fibrosis in the bile duct ligated mouse. J Pharmacol Exp Ther 2004;308(3):1191-6.
  20. Pinzani  M,  Rombouts  K.  Liver  fibrosis:  from  the bench to clinical targets. Dig LiverDis 2004;36(4):231-42.
  21. Elsharkawy AM, Oakley F, Mann DA. The role and regulation of hepatic stellate cell apoptosis in reversal of liver fibrosis. Apoptosis 2005;10(5):927-39.
  22. Mannon RB. Therapeutic targets in the treatment of allograft fibrosis. Am J Transplant 2006;6(5):867-75.
  23. Chapman JR. O’Connell PJ, Nankivell BJ. Chronic Renal Allograft Dysfunction. J Am Soc Nephrol 2005;16(10):3015-26.
  24. Revelo MP, Federspiel C, Helderman H, Fogo AB. Chronic allograft nephropathy: expression and localization of PAI-1 and PPAR-{gamma}. Nephrol Dial Transplant 2005;20(12):2812-9.
  25. Fiorina P, Perseghin G, De Cobelli F, Gremizzi C, Petrelli A, Monti L, et al.Altered Kidney Graft HighEnergy Phosphate Metabolism in Kidney-Transplanted End-Stage Renal Disease Type 1 Diabetic Patients: A cross-sectional analysis of the effect of kidney alone and kidney-pancreas transplantation. Diabetes Care 2007;30(3):597-603.