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.

Bibliographic Details
Main Authors: 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
Format: Article
Language:English
Published: Nature Portfolio 2022-12-01
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.
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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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