Wnt/β-catenin signaling inhibits oxidative stress-induced ferroptosis to improve interstitial cystitis/bladder pain syndrome by reducing NF-κB
Interstitial cystitis/bladder pain syndrome (IC/BPS) is a bladder syndrome of unknown etiology. Reactive oxygen species (ROS) plays a major role in ferroptosis and bladder dysfunction of IC/BPS, while the role of ferroptosis in IC/BPS progression is still unclear. This study aims to investigate the...
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| Veröffentlicht in: | Biochimica et biophysica acta. Molecular cell research 2024-10, Vol.1871 (7), p.119766, Article 119766 |
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| creator | Fang, Weilin Song, Xin Li, Hailong Meng, Fanguo Lv, Tingting Huang, Jin Ji, Xiang Lv, Jianwei Cai, Zhikang Wang, Zhong |
| description | Interstitial cystitis/bladder pain syndrome (IC/BPS) is a bladder syndrome of unknown etiology. Reactive oxygen species (ROS) plays a major role in ferroptosis and bladder dysfunction of IC/BPS, while the role of ferroptosis in IC/BPS progression is still unclear. This study aims to investigate the role and mechanism of ROS-induced ferroptosis in IC/BPS using cell and rat model.
We collected IC/BPS patient bladder tissue samples and established a LPS-induced IC/BPS rat model (LRM). The level of oxidative stress and ferroptosis in IC/BPS patients and LRM rats was analyzed. Function and regulatory mechanism of ferroptosis in IC/BPS were explored by in vitro and in vivo experiments.
The patients with IC/BPS showed mast cells and inflammatory cells infiltration in bladder epithelial tissues. Expression of NRF2 was up-regulated, and GPX4 was decreased in IC/BPS patients compared with normal tissues. IC model cells underwent oxidative stress, which induced ferroptosis. These above results were validated in LRM rat models, and inhibition of ferroptosis ameliorated bladder dysfunction in LRM rats. Wnt/β-catenin signaling was deactivated in IC/BPS patients and animals, and activation of Wnt/β-catenin signaling reduced cellular free radical production, thereby inhibited ferroptosis in IC model cells. Mechanistically, the Wnt/β-catenin signaling pathway inhibited oxidative stress-induced ferroptosis by down-regulating NF-κB, thus contributing to recover IC/BPS both in vitro and in vivo.
We demonstrate for the first time that oxidative stress-induced ferroptosis plays an important role in the pathology of IC/BPS. Mechanistically, the Wnt/β-catenin signaling suppressed oxidative stress-induced ferroptosis by down-regulating NF-κB to improve bladder injury in IC/BPS.
•Bladder tissue of IC/BPS patients exhibits oxidative stress and ferroptosis.•IC model rats/cells undergo oxidative stress which induced ferroptosis.•Inhibition of ferroptosis ameliorates bladder dysfunction in IC/BPS rats.•Wnt/β-catenin signaling deactivates in IC/BPS and activation it inhibited ferroptosis.•Wnt/β-catenin signaling inhibits ROS-induced ferroptosis by NF-κB to recover IC/BPS. |
| doi_str_mv | 10.1016/j.bbamcr.2024.119766 |
| format | Article |
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We collected IC/BPS patient bladder tissue samples and established a LPS-induced IC/BPS rat model (LRM). The level of oxidative stress and ferroptosis in IC/BPS patients and LRM rats was analyzed. Function and regulatory mechanism of ferroptosis in IC/BPS were explored by in vitro and in vivo experiments.
The patients with IC/BPS showed mast cells and inflammatory cells infiltration in bladder epithelial tissues. Expression of NRF2 was up-regulated, and GPX4 was decreased in IC/BPS patients compared with normal tissues. IC model cells underwent oxidative stress, which induced ferroptosis. These above results were validated in LRM rat models, and inhibition of ferroptosis ameliorated bladder dysfunction in LRM rats. Wnt/β-catenin signaling was deactivated in IC/BPS patients and animals, and activation of Wnt/β-catenin signaling reduced cellular free radical production, thereby inhibited ferroptosis in IC model cells. Mechanistically, the Wnt/β-catenin signaling pathway inhibited oxidative stress-induced ferroptosis by down-regulating NF-κB, thus contributing to recover IC/BPS both in vitro and in vivo.
We demonstrate for the first time that oxidative stress-induced ferroptosis plays an important role in the pathology of IC/BPS. Mechanistically, the Wnt/β-catenin signaling suppressed oxidative stress-induced ferroptosis by down-regulating NF-κB to improve bladder injury in IC/BPS.
•Bladder tissue of IC/BPS patients exhibits oxidative stress and ferroptosis.•IC model rats/cells undergo oxidative stress which induced ferroptosis.•Inhibition of ferroptosis ameliorates bladder dysfunction in IC/BPS rats.•Wnt/β-catenin signaling deactivates in IC/BPS and activation it inhibited ferroptosis.•Wnt/β-catenin signaling inhibits ROS-induced ferroptosis by NF-κB to recover IC/BPS.</description><identifier>ISSN: 0167-4889</identifier><identifier>ISSN: 1879-2596</identifier><identifier>EISSN: 1879-2596</identifier><identifier>DOI: 10.1016/j.bbamcr.2024.119766</identifier><identifier>PMID: 38823528</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; beta Catenin - genetics ; beta Catenin - metabolism ; Cystitis, Interstitial - genetics ; Cystitis, Interstitial - metabolism ; Cystitis, Interstitial - pathology ; Disease Models, Animal ; Female ; Ferroptosis ; Humans ; Interstitial cystitis/bladder pain syndrome ; Male ; Middle Aged ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; NF-kappa B - metabolism ; Oxidative Stress ; Phospholipid Hydroperoxide Glutathione Peroxidase - genetics ; Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism ; Rats ; Rats, Sprague-Dawley ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Urinary Bladder - metabolism ; Urinary Bladder - pathology ; Wnt Signaling Pathway ; Wnt/β-catenin signaling</subject><ispartof>Biochimica et biophysica acta. Molecular cell research, 2024-10, Vol.1871 (7), p.119766, Article 119766</ispartof><rights>2024 Elsevier B.V.</rights><rights>Copyright © 2024 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c1568-56cde837f4c7c8e4bd2bb56586bc17eb1bbd5ae9a8321e86770fb872f0087e1e3</cites><orcidid>0000-0002-4931-5543</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbamcr.2024.119766$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38823528$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fang, Weilin</creatorcontrib><creatorcontrib>Song, Xin</creatorcontrib><creatorcontrib>Li, Hailong</creatorcontrib><creatorcontrib>Meng, Fanguo</creatorcontrib><creatorcontrib>Lv, Tingting</creatorcontrib><creatorcontrib>Huang, Jin</creatorcontrib><creatorcontrib>Ji, Xiang</creatorcontrib><creatorcontrib>Lv, Jianwei</creatorcontrib><creatorcontrib>Cai, Zhikang</creatorcontrib><creatorcontrib>Wang, Zhong</creatorcontrib><title>Wnt/β-catenin signaling inhibits oxidative stress-induced ferroptosis to improve interstitial cystitis/bladder pain syndrome by reducing NF-κB</title><title>Biochimica et biophysica acta. Molecular cell research</title><addtitle>Biochim Biophys Acta Mol Cell Res</addtitle><description>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a bladder syndrome of unknown etiology. Reactive oxygen species (ROS) plays a major role in ferroptosis and bladder dysfunction of IC/BPS, while the role of ferroptosis in IC/BPS progression is still unclear. This study aims to investigate the role and mechanism of ROS-induced ferroptosis in IC/BPS using cell and rat model.
We collected IC/BPS patient bladder tissue samples and established a LPS-induced IC/BPS rat model (LRM). The level of oxidative stress and ferroptosis in IC/BPS patients and LRM rats was analyzed. Function and regulatory mechanism of ferroptosis in IC/BPS were explored by in vitro and in vivo experiments.
The patients with IC/BPS showed mast cells and inflammatory cells infiltration in bladder epithelial tissues. Expression of NRF2 was up-regulated, and GPX4 was decreased in IC/BPS patients compared with normal tissues. IC model cells underwent oxidative stress, which induced ferroptosis. These above results were validated in LRM rat models, and inhibition of ferroptosis ameliorated bladder dysfunction in LRM rats. Wnt/β-catenin signaling was deactivated in IC/BPS patients and animals, and activation of Wnt/β-catenin signaling reduced cellular free radical production, thereby inhibited ferroptosis in IC model cells. Mechanistically, the Wnt/β-catenin signaling pathway inhibited oxidative stress-induced ferroptosis by down-regulating NF-κB, thus contributing to recover IC/BPS both in vitro and in vivo.
We demonstrate for the first time that oxidative stress-induced ferroptosis plays an important role in the pathology of IC/BPS. Mechanistically, the Wnt/β-catenin signaling suppressed oxidative stress-induced ferroptosis by down-regulating NF-κB to improve bladder injury in IC/BPS.
•Bladder tissue of IC/BPS patients exhibits oxidative stress and ferroptosis.•IC model rats/cells undergo oxidative stress which induced ferroptosis.•Inhibition of ferroptosis ameliorates bladder dysfunction in IC/BPS rats.•Wnt/β-catenin signaling deactivates in IC/BPS and activation it inhibited ferroptosis.•Wnt/β-catenin signaling inhibits ROS-induced ferroptosis by NF-κB to recover IC/BPS.</description><subject>Animals</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Cystitis, Interstitial - genetics</subject><subject>Cystitis, Interstitial - metabolism</subject><subject>Cystitis, Interstitial - pathology</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Ferroptosis</subject><subject>Humans</subject><subject>Interstitial cystitis/bladder pain syndrome</subject><subject>Male</subject><subject>Middle Aged</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Oxidative Stress</subject><subject>Phospholipid Hydroperoxide Glutathione Peroxidase - genetics</subject><subject>Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Urinary Bladder - metabolism</subject><subject>Urinary Bladder - pathology</subject><subject>Wnt Signaling Pathway</subject><subject>Wnt/β-catenin signaling</subject><issn>0167-4889</issn><issn>1879-2596</issn><issn>1879-2596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1uFDEQhS1ERIbADRDykk3PtPvHdm-QICKAFCUbEEvLP9WhRt32YHuizC04C0sOkTPhoUOW1Ma1-Oq9cj1CXrF6zWrGN9u1MXq2cd3UTbdmbBCcPyErJsVQNf3An5JVwUTVSTmckucpbetSneifkdNWyqbtG7kiP7_5vLn_VVmdwaOnCW-8ntDfUPTf0WBONNyh0xlvgaYcIaUKvdtbcHSEGMMuh4SJ5kBx3sVQKPQZYsqYUU_UHv52aWMm7RxEutNHl4N3McxAzYFGKGpHw6uL6v73-xfkZNRTgpcP7xn5evHhy_mn6vL64-fzd5eVZT2XVc-tA9mKsbPCSuiMa4zpeS-5sUyAYca4XsOgZdswkFyIejRSNGNdSwEM2jPyZtEtS__YQ8pqxmRhmrSHsE-qrXnbCVYUC9otqI0hpQij2kWcdTwoVqtjFmqrlizUMQu1ZFHGXj847M0M7nHo3_EL8HYBoPzzFiGqZBF8OS1GsFm5gP93-AM78aHk</recordid><startdate>202410</startdate><enddate>202410</enddate><creator>Fang, Weilin</creator><creator>Song, Xin</creator><creator>Li, Hailong</creator><creator>Meng, Fanguo</creator><creator>Lv, Tingting</creator><creator>Huang, Jin</creator><creator>Ji, Xiang</creator><creator>Lv, Jianwei</creator><creator>Cai, Zhikang</creator><creator>Wang, Zhong</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4931-5543</orcidid></search><sort><creationdate>202410</creationdate><title>Wnt/β-catenin signaling inhibits oxidative stress-induced ferroptosis to improve interstitial cystitis/bladder pain syndrome by reducing NF-κB</title><author>Fang, Weilin ; Song, Xin ; Li, Hailong ; Meng, Fanguo ; Lv, Tingting ; Huang, Jin ; Ji, Xiang ; Lv, Jianwei ; Cai, Zhikang ; Wang, Zhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1568-56cde837f4c7c8e4bd2bb56586bc17eb1bbd5ae9a8321e86770fb872f0087e1e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>beta Catenin - genetics</topic><topic>beta Catenin - metabolism</topic><topic>Cystitis, Interstitial - genetics</topic><topic>Cystitis, Interstitial - metabolism</topic><topic>Cystitis, Interstitial - pathology</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Ferroptosis</topic><topic>Humans</topic><topic>Interstitial cystitis/bladder pain syndrome</topic><topic>Male</topic><topic>Middle Aged</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Oxidative Stress</topic><topic>Phospholipid Hydroperoxide Glutathione Peroxidase - genetics</topic><topic>Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Urinary Bladder - metabolism</topic><topic>Urinary Bladder - pathology</topic><topic>Wnt Signaling Pathway</topic><topic>Wnt/β-catenin signaling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fang, Weilin</creatorcontrib><creatorcontrib>Song, Xin</creatorcontrib><creatorcontrib>Li, Hailong</creatorcontrib><creatorcontrib>Meng, Fanguo</creatorcontrib><creatorcontrib>Lv, Tingting</creatorcontrib><creatorcontrib>Huang, Jin</creatorcontrib><creatorcontrib>Ji, Xiang</creatorcontrib><creatorcontrib>Lv, Jianwei</creatorcontrib><creatorcontrib>Cai, Zhikang</creatorcontrib><creatorcontrib>Wang, Zhong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochimica et biophysica acta. Molecular cell research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fang, Weilin</au><au>Song, Xin</au><au>Li, Hailong</au><au>Meng, Fanguo</au><au>Lv, Tingting</au><au>Huang, Jin</au><au>Ji, Xiang</au><au>Lv, Jianwei</au><au>Cai, Zhikang</au><au>Wang, Zhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Wnt/β-catenin signaling inhibits oxidative stress-induced ferroptosis to improve interstitial cystitis/bladder pain syndrome by reducing NF-κB</atitle><jtitle>Biochimica et biophysica acta. Molecular cell research</jtitle><addtitle>Biochim Biophys Acta Mol Cell Res</addtitle><date>2024-10</date><risdate>2024</risdate><volume>1871</volume><issue>7</issue><spage>119766</spage><pages>119766-</pages><artnum>119766</artnum><issn>0167-4889</issn><issn>1879-2596</issn><eissn>1879-2596</eissn><abstract>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a bladder syndrome of unknown etiology. Reactive oxygen species (ROS) plays a major role in ferroptosis and bladder dysfunction of IC/BPS, while the role of ferroptosis in IC/BPS progression is still unclear. This study aims to investigate the role and mechanism of ROS-induced ferroptosis in IC/BPS using cell and rat model.
We collected IC/BPS patient bladder tissue samples and established a LPS-induced IC/BPS rat model (LRM). The level of oxidative stress and ferroptosis in IC/BPS patients and LRM rats was analyzed. Function and regulatory mechanism of ferroptosis in IC/BPS were explored by in vitro and in vivo experiments.
The patients with IC/BPS showed mast cells and inflammatory cells infiltration in bladder epithelial tissues. Expression of NRF2 was up-regulated, and GPX4 was decreased in IC/BPS patients compared with normal tissues. IC model cells underwent oxidative stress, which induced ferroptosis. These above results were validated in LRM rat models, and inhibition of ferroptosis ameliorated bladder dysfunction in LRM rats. Wnt/β-catenin signaling was deactivated in IC/BPS patients and animals, and activation of Wnt/β-catenin signaling reduced cellular free radical production, thereby inhibited ferroptosis in IC model cells. Mechanistically, the Wnt/β-catenin signaling pathway inhibited oxidative stress-induced ferroptosis by down-regulating NF-κB, thus contributing to recover IC/BPS both in vitro and in vivo.
We demonstrate for the first time that oxidative stress-induced ferroptosis plays an important role in the pathology of IC/BPS. Mechanistically, the Wnt/β-catenin signaling suppressed oxidative stress-induced ferroptosis by down-regulating NF-κB to improve bladder injury in IC/BPS.
•Bladder tissue of IC/BPS patients exhibits oxidative stress and ferroptosis.•IC model rats/cells undergo oxidative stress which induced ferroptosis.•Inhibition of ferroptosis ameliorates bladder dysfunction in IC/BPS rats.•Wnt/β-catenin signaling deactivates in IC/BPS and activation it inhibited ferroptosis.•Wnt/β-catenin signaling inhibits ROS-induced ferroptosis by NF-κB to recover IC/BPS.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>38823528</pmid><doi>10.1016/j.bbamcr.2024.119766</doi><orcidid>https://orcid.org/0000-0002-4931-5543</orcidid></addata></record> |
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| subjects | Animals beta Catenin - genetics beta Catenin - metabolism Cystitis, Interstitial - genetics Cystitis, Interstitial - metabolism Cystitis, Interstitial - pathology Disease Models, Animal Female Ferroptosis Humans Interstitial cystitis/bladder pain syndrome Male Middle Aged NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism NF-kappa B - metabolism Oxidative Stress Phospholipid Hydroperoxide Glutathione Peroxidase - genetics Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism Rats Rats, Sprague-Dawley Reactive oxygen species Reactive Oxygen Species - metabolism Urinary Bladder - metabolism Urinary Bladder - pathology Wnt Signaling Pathway Wnt/β-catenin signaling |
| title | Wnt/β-catenin signaling inhibits oxidative stress-induced ferroptosis to improve interstitial cystitis/bladder pain syndrome by reducing NF-κB |
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