dc.contributor.author | Tang, Y | |
dc.contributor.author | Wu, J | |
dc.contributor.author | Sun, X | |
dc.contributor.author | Tan, S | |
dc.contributor.author | Li, W | |
dc.contributor.author | Yin, S | |
dc.contributor.author | Liu, L | |
dc.contributor.author | Chen, Y | |
dc.contributor.author | Liu, Y | |
dc.contributor.author | Tan, Q | |
dc.contributor.author | Jiang, Y | |
dc.contributor.author | Yang, W | |
dc.contributor.author | Huang, W | |
dc.contributor.author | Weng, C | |
dc.contributor.author | Wu, Q | |
dc.contributor.author | Lu, Y | |
dc.contributor.author | Yuan, H | |
dc.contributor.author | Xiao, Q | |
dc.contributor.author | Chen, AF | |
dc.contributor.author | Xu, Q | |
dc.contributor.author | Billiar, TR | |
dc.contributor.author | Cai, J | |
dc.date.accessioned | 2024-05-20T07:25:35Z | |
dc.date.available | 2024-04-30 | |
dc.date.available | 2024-05-20T07:25:35Z | |
dc.date.issued | 2024-05-15 | |
dc.identifier.citation | TY - JOUR T1 - Cardiolipin oxidized by ROS from complex II acts as a target of gasdermin D to drive mitochondrial pore and heart dysfunction in endotoxemia AU - Tang, Yan AU - Wu, Junru AU - Sun, Xuejing AU - Tan, Shasha AU - Li, Wenbo AU - Yin, Siyu AU - Liu, Lun AU - Chen, Yuanyuan AU - Liu, Yuanyuan AU - Tan, Qian AU - Jiang, Youxiang AU - Yang, Wenjing AU - Huang, Wei AU - Weng, Chunyan AU - Wu, Qing AU - Lu, Yao AU - Yuan, Hong AU - Xiao, Qingzhong AU - Chen, Alex F. AU - Xu, Qingbo AU - Billiar, Timothy R. AU - Cai, Jingjing Y1 - 2024/05/28 PY - 2024 N1 - doi: 10.1016/j.celrep.2024.114237 DO - 10.1016/j.celrep.2024.114237 T2 - Cell Reports JF - Cell Reports VL - 43 IS - 5 PB - Elsevier SN - 2211-1247 M3 - doi: 10.1016/j.celrep.2024.114237 UR - https://doi.org/10.1016/j.celrep.2024.114237 Y2 - 2024/05/20 ER - | en_US |
dc.identifier.uri | https://qmro.qmul.ac.uk/xmlui/handle/123456789/96959 | |
dc.description.abstract | Cardiac dysfunction, an early complication of endotoxemia, is the major cause of death in intensive care units. No specific therapy is available at present for this cardiac dysfunction. Here, we show that the N-terminal gasdermin D (GSDMD-N) initiates mitochondrial apoptotic pore and cardiac dysfunction by directly interacting with cardiolipin oxidized by complex II-generated reactive oxygen species (ROS) during endotoxemia. Caspase-4/11 initiates GSDMD-N pores that are subsequently amplified by the upregulation and activation of NLRP3 inflammation through further generation of ROS. GSDMD-N pores form prior to BAX and VDAC1 apoptotic pores and further incorporate into BAX and VDAC1 oligomers within mitochondria membranes to exacerbate the apoptotic process. Our findings identify oxidized cardiolipin as the definitive target of GSDMD-N in mitochondria of cardiomyocytes during endotoxin-induced myocardial dysfunction (EIMD), and modulation of cardiolipin oxidation could be a therapeutic target early in the disease process to prevent EIMD. | en_US |
dc.format.extent | 114237 - ? | |
dc.language | eng | |
dc.publisher | Cell Press | en_US |
dc.relation.ispartof | Cell Rep | |
dc.rights | This is an open access article under the CC BY-NC license (http://creativecommons.org/licenses/by-nc/4.0/). | |
dc.subject | CP: Immunology | en_US |
dc.subject | cardiolipin | en_US |
dc.subject | complex II | en_US |
dc.subject | endotoxin-induced myocardial dysfunction | en_US |
dc.subject | gasdermin D | en_US |
dc.subject | mitochondria | en_US |
dc.title | Cardiolipin oxidized by ROS from complex II acts as a target of gasdermin D to drive mitochondrial pore and heart dysfunction in endotoxemia. | en_US |
dc.type | Article | en_US |
dc.rights.holder | © 2024 The Author(s). Published by Elsevier Inc. 1 | |
dc.identifier.doi | 10.1016/j.celrep.2024.114237 | |
pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/38753484 | en_US |
pubs.issue | 5 | en_US |
pubs.notes | Not known | en_US |
pubs.publication-status | Published online | en_US |
pubs.volume | 43 | en_US |
dcterms.dateAccepted | 2024-04-30 | |
rioxxterms.funder | Default funder | en_US |
rioxxterms.identifier.project | Default project | en_US |
qmul.funder | A novel role for CD34+ cell-derived fibroblasts in abdominal aortic aneurysm::British Heart Foundation | en_US |
qmul.funder | A novel role for CD34+ cell-derived fibroblasts in abdominal aortic aneurysm::British Heart Foundation | en_US |
qmul.funder | A novel role for CD34+ cell-derived fibroblasts in abdominal aortic aneurysm::British Heart Foundation | en_US |
qmul.funder | A novel role for CD34+ cell-derived fibroblasts in abdominal aortic aneurysm::British Heart Foundation | en_US |