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Review
. 2019 Jul 15;200(2):140-151.
doi: 10.1164/rccm.201903-0497PP.

Is Progression of Pulmonary Fibrosis due to Ventilation-induced Lung Injury?

Richard K Albert  1 , Bradford Smith  2 , Carrie E Perlman  3 , David A Schwartz  1
Affiliations
Review

Is Progression of Pulmonary Fibrosis due to Ventilation-induced Lung Injury?

Richard K Albert et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Proposed pathogenesis of pulmonary fibrosis (PF) progression resulting from ventilation-induced lung injury (VILI). Surfactant abnormalities can occur directly (e.g., surfactant gene variant and smoking) or indirectly as a result of alveolar type II cell injury, which, in turn, can also occur directly (e.g., radiation) and/or through endoplasmic reticulum (ER) stress (e.g., SP-A or SP-C mutations). Mechanotransduction can cause progression of fibrosis by several mechanisms, including directly damaging cell membranes, changing the cytoskeletal structure, and/or activating ion channels. Each of these effects activates different signaling pathways, resulting in production and release of cytokines and chemokines, ER stress, and/or epithelial–mesenchymal transition (EMT). GERD = gastroesophageal reflux disease; TGF-β = transforming growth factor-β.
Figure 2.
Figure 2.
Maximum alveolar septal strain (εmax) increases with alveolar collapse. (A) The undeformed finite element domain represents the linear elastic alveolar network at FRC. (B) Tripling the lung volume above the resting state, which we equate to a deep inspiration (e.g., TLC), corresponds to a cross-sectional area that is 32/3 times that at FRC, assuming that the expansion of the lung is isotropic. (F) Stiffening a single alveolus by a factor of 100 to simulate flooding (gray) does not affect strain at FRC and causes a moderate increase at TLC. (C and F) A collapsed and stiffened (i.e., atelectatic) alveolus is represented by reducing the resting area by 90% and increasing the elastic modulus 100-fold (C) to yield an εmax at FRC that is approximately equal to εmax at TLC in the open network (F). (D) Inflating the network to TLC with a single atelectatic alveolus yields a 2.5-fold increase in εmax compared with the open network. (E and F) Increasing the number of atelectatic alveoli (E) increases εmax at both FRC and TLC compared with a single collapsed alveolus (F). The color bar indicates strain in the alveolar septa shown in A–E.
See this image and copyright information in PMC

References

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