https://scholars.lib.ntu.edu.tw/handle/123456789/462948
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Hsu, Y.-H. | en_US |
dc.contributor.author | Chuang, H.-C. | en_US |
dc.contributor.author | Lee, Y.-H. | en_US |
dc.contributor.author | Lin, Y.-F. | en_US |
dc.contributor.author | Chen, Y.-J. | en_US |
dc.contributor.author | Hsiao, T.-C. | en_US |
dc.contributor.author | Wu, M.-Y. | en_US |
dc.contributor.author | Chiu, H.-W. | en_US |
dc.contributor.author | TA-CHIH HSIAO | en_US |
dc.creator | TA-CHIH HSIAO;Chiu, H.-W.;Wu, M.-Y.;Hsiao, T.-C.;Chen, Y.-J.;Lin, Y.-F.;Lee, Y.-H.;Chuang, H.-C.;Hsu, Y.-H. | - |
dc.date.accessioned | 2020-02-25T06:10:52Z | - |
dc.date.available | 2020-02-25T06:10:52Z | - |
dc.date.issued | 2019 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/462948 | - |
dc.description.abstract | Traffic emission is responsible for most small-sized particulate matter (PM) air pollution in urban areas. Several recent studies have indicated that traffic-related PM may aggravate kidney disease. Furthermore, exposure to particulate air pollution may be related to the risk of chronic kidney disease (CKD). However, the underlying molecular mechanisms have not been adequately addressed. In the present study, we studied the mechanisms of renal damage that might be associated with exposure to PM. In a real world of whole-body exposure to traffic-related PM model for 3–6 months, PM in urban ambient air can affect kidney function and induce autophagy, endoplasmic reticulum (ER) stress and apoptosis in kidney tissues. Exposure to traffic-related diesel particulate matter (DPM) led to a reduction in cell viability in human kidney tubular epithelial cells HK-2. DPM increased mitochondrial reactive oxygen species (ROS) and decreased the mitochondrial membrane potential. Furthermore, DPM induced ER stress and activated the unfolded protein response (UPR) pathway. Eventually, DPM exposure induced caspase pathways and triggered apoptosis. In addition, DPM induced autophagy through the inhibition of the Akt/mTOR pathway. Autophagy inhibition resulted in significantly increased cytotoxicity and apoptosis. These findings suggest that air pollution in urban areas may cause nephrotoxicity and autophagy as a protective role in PM-induced cytotoxicity. © 2019 The Authors | - |
dc.relation.ispartof | Free Radical Biology and Medicine | - |
dc.subject | Apoptosis; Autophagy; Endoplasmic reticulum stress; Nephrotoxicity | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.classification | [SDGs]SDG11 | - |
dc.subject.other | caspase; creatinine; cystatin C; diesel fuel; mammalian target of rapamycin; nitrogen; protein kinase B; reactive oxygen metabolite; urea; caspase; MTOR protein, human; protein kinase B; reactive oxygen metabolite; target of rapamycin kinase; air pollution; ambient air; animal experiment; animal model; animal tissue; apoptosis; Article; autophagy; cell viability; chronic kidney failure; controlled study; cytotoxicity; disease association; disease exacerbation; endoplasmic reticulum stress; environmental exposure; enzyme induction; epithelium cell; exhaust gas; human; human cell; in vitro study; in vivo study; kidney function; kidney tissue; kidney tubule epithelium; mitochondrial membrane potential; mitochondrion; molecular mechanics; nephrotoxicity; nonhuman; particulate matter; priority journal; rat; unfolded protein response; urban area; air pollutant; animal; autophagy; cell line; cell survival; drug effect; exhaust gas; genetics; kidney; metabolism; oxidative stress; particulate matter; pathology; toxicity; Air Pollutants; Animals; Apoptosis; Autophagy; Caspases; Cell Line; Cell Survival; Endoplasmic Reticulum Stress; Humans; Kidney; Mitochondria; Oxidative Stress; Particulate Matter; Proto-Oncogene Proteins c-akt; Rats; Reactive Oxygen Species; Renal Insufficiency, Chronic; TOR Serine-Threonine Kinases; Unfolded Protein Response; Vehicle Emissions | - |
dc.title | Traffic-related particulate matter exposure induces nephrotoxicity in vitro and in vivo | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1016/j.freeradbiomed.2019.03.008 | - |
dc.identifier.scopus | 2-s2.0-85062945473 | - |
dc.identifier.url | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85062945473&doi=10.1016%2fj.freeradbiomed.2019.03.008&partnerID=40&md5=d23ab64c05884870b5fab45fc2f89b96 | - |
dc.relation.pages | 235-244 | - |
dc.relation.journalvolume | 135 | - |
item.openairetype | journal article | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Environmental Engineering | - |
crisitem.author.parentorg | College of Engineering | - |
顯示於: | 環境工程學研究所 |
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