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X Demographics
Mendeley readers
Attention Score in Context
| Title |
Pirfenidone inhibits myofibroblast differentiation and lung fibrosis development during insufficient mitophagy
|
|---|---|
| Published in |
Respiratory Research, June 2017
|
| DOI | 10.1186/s12931-017-0600-3 |
| Pubmed ID | |
| Authors |
Yusuke Kurita, Jun Araya, Shunsuke Minagawa, Hiromichi Hara, Akihiro Ichikawa, Nayuta Saito, Tsukasa Kadota, Kazuya Tsubouchi, Nahoko Sato, Masahiro Yoshida, Kenji Kobayashi, Saburo Ito, Yu Fujita, Hirofumi Utsumi, Haruhiko Yanagisawa, Mitsuo Hashimoto, Hiroshi Wakui, Yutaka Yoshii, Takeo Ishikawa, Takanori Numata, Yumi Kaneko, Hisatoshi Asano, Makoto Yamashita, Makoto Odaka, Toshiaki Morikawa, Katsutoshi Nakayama, Kazuyoshi Kuwano |
| Abstract |
Pirfenidone (PFD) is an anti-fibrotic agent used to treat idiopathic pulmonary fibrosis (IPF), but its precise mechanism of action remains elusive. Accumulation of profibrotic myofibroblasts is a crucial process for fibrotic remodeling in IPF. Recent findings show participation of autophagy/mitophagy, part of the lysosomal degradation machinery, in IPF pathogenesis. Mitophagy has been implicated in myofibroblast differentiation through regulating mitochondrial reactive oxygen species (ROS)-mediated platelet-derived growth factor receptor (PDGFR) activation. In this study, the effect of PFD on autophagy/mitophagy activation in lung fibroblasts (LF) was evaluated, specifically the anti-fibrotic property of PFD for modulation of myofibroblast differentiation during insufficient mitophagy. Transforming growth factor-β (TGF-β)-induced or ATG5, ATG7, and PARK2 knockdown-mediated myofibroblast differentiation in LF were used for in vitro models. The anti-fibrotic role of PFD was examined in a bleomycin (BLM)-induced lung fibrosis model using PARK2 knockout (KO) mice. We found that PFD induced autophagy/mitophagy activation via enhanced PARK2 expression, which was partly involved in the inhibition of myofibroblast differentiation in the presence of TGF-β. PFD inhibited the myofibroblast differentiation induced by PARK2 knockdown by reducing mitochondrial ROS and PDGFR-PI3K-Akt activation. BLM-treated PARK2 KO mice demonstrated augmentation of lung fibrosis and oxidative modifications compared to those of BLM-treated wild type mice, which were efficiently attenuated by PFD. These results suggest that PFD induces PARK2-mediated mitophagy and also inhibits lung fibrosis development in the setting of insufficient mitophagy, which may at least partly explain the anti-fibrotic mechanisms of PFD for IPF treatment. |
X Demographics
The data shown below were collected from the profiles of 20 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| United Kingdom | 4 | 20% |
| France | 2 | 10% |
| Canada | 2 | 10% |
| Colombia | 1 | 5% |
| United States | 1 | 5% |
| Unknown | 10 | 50% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 13 | 65% |
| Practitioners (doctors, other healthcare professionals) | 6 | 30% |
| Scientists | 1 | 5% |
Mendeley readers
The data shown below were compiled from readership statistics for 65 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 65 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 14 | 22% |
| Student > Ph. D. Student | 7 | 11% |
| Student > Doctoral Student | 5 | 8% |
| Lecturer | 4 | 6% |
| Student > Bachelor | 4 | 6% |
| Other | 8 | 12% |
| Unknown | 23 | 35% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 14 | 22% |
| Biochemistry, Genetics and Molecular Biology | 10 | 15% |
| Agricultural and Biological Sciences | 8 | 12% |
| Pharmacology, Toxicology and Pharmaceutical Science | 3 | 5% |
| Immunology and Microbiology | 2 | 3% |
| Other | 3 | 5% |
| Unknown | 25 | 38% |
Attention Score in Context
This research output has an Altmetric Attention Score of 19. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 July 2017.
All research outputs
#1,980,997
of 25,382,440 outputs
Outputs from Respiratory Research
#185
of 3,062 outputs
Outputs of similar age
#37,537
of 331,648 outputs
Outputs of similar age from Respiratory Research
#11
of 79 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 92nd percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 3,062 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.9. This one has done particularly well, scoring higher than 93% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 331,648 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 88% of its contemporaries.
We're also able to compare this research output to 79 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 86% of its contemporaries.