TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage
TRPCs, nonselective cation channels, are involved in cardiac contraction and conduction. Here, the authors show that Trpc1/6 deficiency or pharmacological inhibition improves endotoxemic cardiac dysfunction and prolongs survival by prominently suppressing cardiac inflammation and ER Ca2+ release.
Main Authors: | , , , , , , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2022-12-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-022-35242-0 |
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author | Na Tang Wen Tian Guang-Yuan Ma Xiong Xiao Lei Zhou Ze-Zhi Li Xiao-Xiao Liu Chong-Yao Li Ke-Han Wu Wenjuan Liu Xue-Ying Wang Yuan-Yuan Gao Xin Yang Jianzhao Qi Ding Li Yang Liu Wen-Sheng Chen Jinming Gao Xiao-Qiang Li Wei Cao |
author_facet | Na Tang Wen Tian Guang-Yuan Ma Xiong Xiao Lei Zhou Ze-Zhi Li Xiao-Xiao Liu Chong-Yao Li Ke-Han Wu Wenjuan Liu Xue-Ying Wang Yuan-Yuan Gao Xin Yang Jianzhao Qi Ding Li Yang Liu Wen-Sheng Chen Jinming Gao Xiao-Qiang Li Wei Cao |
author_sort | Na Tang |
collection | DOAJ |
description | TRPCs, nonselective cation channels, are involved in cardiac contraction and conduction. Here, the authors show that Trpc1/6 deficiency or pharmacological inhibition improves endotoxemic cardiac dysfunction and prolongs survival by prominently suppressing cardiac inflammation and ER Ca2+ release. |
first_indexed | 2024-04-12T04:09:32Z |
format | Article |
id | doaj.art-1f2bcaf485214c439faec467d7e47ea1 |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-04-12T04:09:32Z |
publishDate | 2022-12-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
spelling | doaj.art-1f2bcaf485214c439faec467d7e47ea12022-12-22T03:48:32ZengNature PortfolioNature Communications2041-17232022-12-0113112110.1038/s41467-022-35242-0TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakageNa Tang0Wen Tian1Guang-Yuan Ma2Xiong Xiao3Lei Zhou4Ze-Zhi Li5Xiao-Xiao Liu6Chong-Yao Li7Ke-Han Wu8Wenjuan Liu9Xue-Ying Wang10Yuan-Yuan Gao11Xin Yang12Jianzhao Qi13Ding Li14Yang Liu15Wen-Sheng Chen16Jinming Gao17Xiao-Qiang Li18Wei Cao19Department of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical UniversityDepartment of Pharmacy, Xi’an No.3 Hospital, the Affiliated Hospital of Northwest UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical UniversityDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityShaanxi Key Laboratory of Natural Products & Chemical Biology, Northwest A&F UniversityShaanxi Key Laboratory of Natural Products & Chemical Biology, Northwest A&F UniversityDepartment of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical UniversityDepartment of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical UniversityDepartment of Pharmacy, School of Chemistry & Pharmacy, Northwest A&F UniversityTRPCs, nonselective cation channels, are involved in cardiac contraction and conduction. Here, the authors show that Trpc1/6 deficiency or pharmacological inhibition improves endotoxemic cardiac dysfunction and prolongs survival by prominently suppressing cardiac inflammation and ER Ca2+ release.https://doi.org/10.1038/s41467-022-35242-0 |
spellingShingle | Na Tang Wen Tian Guang-Yuan Ma Xiong Xiao Lei Zhou Ze-Zhi Li Xiao-Xiao Liu Chong-Yao Li Ke-Han Wu Wenjuan Liu Xue-Ying Wang Yuan-Yuan Gao Xin Yang Jianzhao Qi Ding Li Yang Liu Wen-Sheng Chen Jinming Gao Xiao-Qiang Li Wei Cao TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage Nature Communications |
title | TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage |
title_full | TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage |
title_fullStr | TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage |
title_full_unstemmed | TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage |
title_short | TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage |
title_sort | trpc channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and ca2 leakage |
url | https://doi.org/10.1038/s41467-022-35242-0 |
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