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. 2020 Sep 4;8:819. doi: 10.3389/fcell.2020.00819

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Copyright © 2020 Jing, Hu, Lin, He, Zhang, Ge, Dai, Du, Lin and Pan.

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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Schematic illustrating a potential pathway from cyclic stretching (CS) to inflammation and injury in lung epithelial cells via Toll-like receptor (TLR)-9 stimulation and release of mitochondrial DNA (mtDNA). Exposure of excessive CS triggers mitochondrial damage that is degraded by activated mitophagy. Subsequently, mtDNA is released from degraded mitochondria to extracellular fluid, then it is recognized and combined with TLR-9 in the other normal cells. TLR9 interacts with myeloid differentiation primary response 88 (MyD88) through downstream TLR9/MyD88 signaling. This pathway finally leads to activating nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and translation of proinflammatory cytokines. Proinflammatory cytokines are then matured and transformed into inflammatory cytokines for cascade amplification of inflammatory response and cell injury.