Mitochondrial dysfunction contributes to the senescent phenotype of IPF lung fibroblasts.

In conclusion, increased superoxide production by dysfunctional mitochondria reinforces lung fibroblast senescence via prolongation of the DDR. As part of an auto-amplifying loop, mTORC1 is activated, altering mitochondrial homoeostasis and increasing superoxide production. Deeper understanding the mechanisms by which mitochondria contribute to fibroblast senescence in IPF has potentially important therapeutic implications.
PMID: 30255990 [PubMed - as supplied by publisher]

Source: J Cell Mol Med - September 26, 2018 Category: Molecular Biology Authors: Schuliga M, Pechkovsky DV, Read J, Waters DW, Blokland KEC, Reid AT, Hogaboam CM, Khalil N, Burgess JK, Prêle CM, Mutsaers SE, Jaffar J, Westall G, Grainge C, Knight DA Tags: J Cell Mol Med Source Type: research