Potential therapeutic initiatives for fibrogenic lung diseases.
Fibrotic process affecting the lung and other tissues is characterized by stimulation of fibroblast proliferation and connective tissue deposition. Conventional therapy consisting of glucocorticoids or cytotoxic agents is usually ineffective in blocking progression of disease. Potential new therapies have emerged from the use of animal models of pulmonary fibrosis and recent advances in the cellular and molecular biology of inflammatory reactions. Such therapies involve the use of substances directed against the action of certain growth factors, cytokines, or oxidants that are elaborated during the fibrotic reaction. In this article, we review possible therapeutic applications of these advances.
Goldstein
R H
RH
Pulmonary Center, Boston University School of Medicine, MA 02118, USA.
Fine
A
A
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D003094:Collagen / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D004195:Disease Models, Animal; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000627:therapeutic use; D006801:Humans; D007375:Interleukin-1 / Q000037:antagonists & inhibitors; D011658:Pulmonary Fibrosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D017382:Reactive Oxygen Species; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D000806:Angiotensin-Converting Enzyme Inhibitors; D000975:Antioxidants; D007375:Interleukin-1; D017382:Reactive Oxygen Species; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D003094:Collagen