Cardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis
Ca2+ overload and mitochondrial dysfunction play crucial roles in myocardial ischemia-reperfusion (I/R) injury. Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca2+ homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function du...
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| Veröffentlicht in: | Redox biology 2025-02, Vol.79, p.103471, Article 103471 |
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| creator | Xu, Honglin Chen, Xin Luo, Shangfei Jiang, Jintao Pan, Xianmei He, Yu Deng, Bo Liu, Silin Wan, Rentao Lin, Liwen Tan, Qiaorui Chen, Xiaoting Yao, Youfen He, Bin An, Yajuan Li, Jing |
| description | Ca2+ overload and mitochondrial dysfunction play crucial roles in myocardial ischemia-reperfusion (I/R) injury. Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca2+ homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function during myocardial I/R injury. We showed that the expression of myocardial Piezo1 was elevated in the infracted area of I/R and cardiomyocyte-specific Piezo1 deficiency (Piezo1△Myh6) mice attenuated I/R by decreasing infarct size and cardiac dysfunction. Piezo1△Myh6 regulated mitochondrial fusion and fission to improve mitochondrial function and decrease inflammation and oxidative stress in vivo and in vitro. Mechanistically, myocardial Piezo1 knockout alleviated intracellular calcium overload to normalize calpain-associated mitochondrial homeostasis. Our findings indicated that Piezo1 depletion in cardiomyocytes partially restored mitochondrial homeostasis during cardiac ischemia/reperfusion (I/R) injury. This study suggests an innovative therapeutic strategy to alleviate cardiac I/R injury. |
| doi_str_mv | 10.1016/j.redox.2024.103471 |
| format | Article |
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Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca2+ homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function during myocardial I/R injury. We showed that the expression of myocardial Piezo1 was elevated in the infracted area of I/R and cardiomyocyte-specific Piezo1 deficiency (Piezo1△Myh6) mice attenuated I/R by decreasing infarct size and cardiac dysfunction. Piezo1△Myh6 regulated mitochondrial fusion and fission to improve mitochondrial function and decrease inflammation and oxidative stress in vivo and in vitro. Mechanistically, myocardial Piezo1 knockout alleviated intracellular calcium overload to normalize calpain-associated mitochondrial homeostasis. Our findings indicated that Piezo1 depletion in cardiomyocytes partially restored mitochondrial homeostasis during cardiac ischemia/reperfusion (I/R) injury. This study suggests an innovative therapeutic strategy to alleviate cardiac I/R injury.</description><identifier>ISSN: 2213-2317</identifier><identifier>EISSN: 2213-2317</identifier><identifier>DOI: 10.1016/j.redox.2024.103471</identifier><identifier>PMID: 39740362</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Calcium - metabolism ; Calpain ; Cardiomyocytes ; Disease Models, Animal ; Homeostasis ; I/R ; Inflammation ; Ion Channels - genetics ; Ion Channels - metabolism ; Male ; Mice ; Mice, Knockout ; Mitochondria ; Mitochondria - genetics ; Mitochondria - metabolism ; Mitochondrial Dynamics - genetics ; Myocardial Reperfusion Injury - genetics ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Oxidative Stress ; Piezo1 ; Research Paper</subject><ispartof>Redox biology, 2025-02, Vol.79, p.103471, Article 103471</ispartof><rights>2025 The Authors</rights><rights>Copyright © 2025 The Authors. Published by Elsevier B.V. All rights reserved.</rights><rights>2025 The Authors. Published by Elsevier B.V. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2765-3805e69248cb1c1bf0974984eea5d98ba8711a18d7e68895f4dc9b3524d7dd033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11750285/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11750285/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39740362$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Honglin</creatorcontrib><creatorcontrib>Chen, Xin</creatorcontrib><creatorcontrib>Luo, Shangfei</creatorcontrib><creatorcontrib>Jiang, Jintao</creatorcontrib><creatorcontrib>Pan, Xianmei</creatorcontrib><creatorcontrib>He, Yu</creatorcontrib><creatorcontrib>Deng, Bo</creatorcontrib><creatorcontrib>Liu, Silin</creatorcontrib><creatorcontrib>Wan, Rentao</creatorcontrib><creatorcontrib>Lin, Liwen</creatorcontrib><creatorcontrib>Tan, Qiaorui</creatorcontrib><creatorcontrib>Chen, Xiaoting</creatorcontrib><creatorcontrib>Yao, Youfen</creatorcontrib><creatorcontrib>He, Bin</creatorcontrib><creatorcontrib>An, Yajuan</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><title>Cardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis</title><title>Redox biology</title><addtitle>Redox Biol</addtitle><description>Ca2+ overload and mitochondrial dysfunction play crucial roles in myocardial ischemia-reperfusion (I/R) injury. Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca2+ homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function during myocardial I/R injury. We showed that the expression of myocardial Piezo1 was elevated in the infracted area of I/R and cardiomyocyte-specific Piezo1 deficiency (Piezo1△Myh6) mice attenuated I/R by decreasing infarct size and cardiac dysfunction. Piezo1△Myh6 regulated mitochondrial fusion and fission to improve mitochondrial function and decrease inflammation and oxidative stress in vivo and in vitro. Mechanistically, myocardial Piezo1 knockout alleviated intracellular calcium overload to normalize calpain-associated mitochondrial homeostasis. Our findings indicated that Piezo1 depletion in cardiomyocytes partially restored mitochondrial homeostasis during cardiac ischemia/reperfusion (I/R) injury. This study suggests an innovative therapeutic strategy to alleviate cardiac I/R injury.</description><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Calpain</subject><subject>Cardiomyocytes</subject><subject>Disease Models, Animal</subject><subject>Homeostasis</subject><subject>I/R</subject><subject>Inflammation</subject><subject>Ion Channels - genetics</subject><subject>Ion Channels - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mitochondria</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial Dynamics - genetics</subject><subject>Myocardial Reperfusion Injury - genetics</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Oxidative Stress</subject><subject>Piezo1</subject><subject>Research Paper</subject><issn>2213-2317</issn><issn>2213-2317</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNp9Uk1v1DAQjRCIVqW_AAnlyCVbf8Sxc0AIrYBWqgQHOFuOPdmdVRIHO1kRfj3eTanaC77YM5735mnmZdlbSjaU0OrmsAng_O8NI6xMGV5K-iK7ZIzygnEqXz55X2TXMR5IOkqVjJLX2QWvZUl4xS6z49YEh75fvF0mKOIIFlu0-XeEP57mDlKAMNgl73HCnZkg5hjtHno0RYARQjtH9EOOw2EOS94s-RggQjjisDthvN37wQU0Xb73Pfg4mYjxTfaqNV2E64f7Kvv55fOP7W1x_-3r3fbTfWGZrETBFRFQ1axUtqGWNi1JwmtVAhjhatUYJSk1VDkJlVK1aEtn64YLVjrpHOH8KrtbeZ03Bz0G7E1YtDeozwkfdtqECW0H2krKlXKCO7BlA6AcSHAghDGWOMkS18eVa5ybHpyFYQqme0b6_GfAvd75o6ZUCsKUSAzvHxiC_zVDnHSfZgldZwbwc9ScCiIYJ2fhfC21wccYoH3sQ4k-OUAf9NkB-uQAvTogod49lfiI-bfvVPBhLYA09CNC0PG8XnAYwE5pKvjfBn8BQZvHGw</recordid><startdate>202502</startdate><enddate>202502</enddate><creator>Xu, Honglin</creator><creator>Chen, Xin</creator><creator>Luo, Shangfei</creator><creator>Jiang, Jintao</creator><creator>Pan, Xianmei</creator><creator>He, Yu</creator><creator>Deng, Bo</creator><creator>Liu, Silin</creator><creator>Wan, Rentao</creator><creator>Lin, Liwen</creator><creator>Tan, Qiaorui</creator><creator>Chen, Xiaoting</creator><creator>Yao, Youfen</creator><creator>He, Bin</creator><creator>An, Yajuan</creator><creator>Li, Jing</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><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><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>202502</creationdate><title>Cardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis</title><author>Xu, Honglin ; 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Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca2+ homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function during myocardial I/R injury. We showed that the expression of myocardial Piezo1 was elevated in the infracted area of I/R and cardiomyocyte-specific Piezo1 deficiency (Piezo1△Myh6) mice attenuated I/R by decreasing infarct size and cardiac dysfunction. Piezo1△Myh6 regulated mitochondrial fusion and fission to improve mitochondrial function and decrease inflammation and oxidative stress in vivo and in vitro. Mechanistically, myocardial Piezo1 knockout alleviated intracellular calcium overload to normalize calpain-associated mitochondrial homeostasis. Our findings indicated that Piezo1 depletion in cardiomyocytes partially restored mitochondrial homeostasis during cardiac ischemia/reperfusion (I/R) injury. 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| subjects | Animals Calcium - metabolism Calpain Cardiomyocytes Disease Models, Animal Homeostasis I/R Inflammation Ion Channels - genetics Ion Channels - metabolism Male Mice Mice, Knockout Mitochondria Mitochondria - genetics Mitochondria - metabolism Mitochondrial Dynamics - genetics Myocardial Reperfusion Injury - genetics Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Oxidative Stress Piezo1 Research Paper |
| title | Cardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis |
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