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. 2020 Nov 12;7:606462. doi: 10.3389/fmed.2020.606462

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Copyright © 2020 Venosa.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Modeling chemical exposure on the fibrotic phenotype. Depiction of possible outcomes resulting from aging and chemical exposure and their relationship to fibrogenesis. Highly fibrogenic chemical exposure (1, gray dotted line, ) may drive rapid and possibly lethal fibrosis after a single exposure. By comparison, aging may lead to different disease profiles based on factor such as genetic instability (i.e., SP-C mutation). In such case, an individual presenting somatic mutations may be predisposed to develop a fibrotic phenotype without toxic challenge (2a, blue line, ), compared to a healthy individual (2b, blue dotted line, ). Similar responses can be observed following mild/moderate repeated exposure, with susceptible population (3a, red line, ) passing the “fibrogenic threshold", whereas healthy cohorts will not. (3b, red dotted line, ) or never reach that threshold depending on factor such as genetic susceptibility. Similarly, aging may be associated with fibrotic and non-fibrotic outcomes depending on individual biological clocks.

Inline graphic — Modeling chemical exposure on the fibrotic phenotype. Depiction of possible outcomes resulting from aging and chemical exposure and their relationship to fibrogenesis. Highly fibrogenic chemical exposure (1, gray dotted line, ) may drive rapid and possibly lethal fibrosis after a single exposure. By comparison, aging may lead to different disease profiles based on factor such as genetic instability (i.e., SP-C mutation). In such case, an individual presenting somatic mutations may be predisposed to develop a fibrotic phenotype without toxic challenge (2a, blue line, ), compared to a healthy individual (2b, blue dotted line, ). Similar responses can be observed following mild/moderate repeated exposure, with susceptible population (3a, red line, ) passing the “fibrogenic threshold", whereas healthy cohorts will not. (3b, red dotted line, ) or never reach that threshold depending on factor such as genetic susceptibility. Similarly, aging may be associated with fibrotic and non-fibrotic outcomes depending on individual biological clocks.