4.6 Review

Mechanisms of Lung Fibrosis Resolution

Journal

AMERICAN JOURNAL OF PATHOLOGY
Volume 186, Issue 5, Pages 1066-1077

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2016.01.018

Keywords

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Categories

Funding

  1. NIH/National Heart, Lung and Blood Institute (NHLBI) [HL082818, HL111169, R01HIL111169-02S1, U10-HL-101800]
  2. NIH National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) [IR03AR062832-01A1]
  3. NIH National Institute on Aging (NIA) [1R21AG047473-01A1]
  4. Parker B. Francis Fellowship
  5. American Heart Association [12SDG9130040]

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Fibrogenesis involves a dynamic interplay between factors that promote the biosynthesis and deposition of extracellular matrix along with pathways that degrade the extracellular matrix and eliminate the primary effector cells. Opposing the often held perception that fibrotic tissue is permanent, animal studies and clinical data now demonstrate the highly plastic nature of organ fibrosis that can, under certain circumstances, regress. This review describes the current understanding of the mechanisms whereby the lung is known to resolve fibrosis focusing on degradation of the extracellular matrix, removal of myofibroblasts, and the role of inflammatory cells. Although there are significant gaps in understanding Lung fibrosis resolution, accelerated improvements in biotechnology and bioinformatics are expected to improve the understanding of these mechanisms and have high potential to lead to novel and effective restorative therapies in the treatment not only of pulmonary fibrosis, but also of a wide-ranging spectrum of chronic disorders.

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