http://purl.uniprot.org/citations/33619515 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/33619515 | http://www.w3.org/2000/01/rdf-schema#comment | "Mitochondrial reactive oxygen species (mtROS)-induced apoptosis has been suggested to contribute to myocardial ischemia/reperfusion injury. Interleukin 35 (IL-35), a novel anti-inflammatory cytokine, has been shown to protect the myocardium and inhibit mtROS production. However, its effect on cardiomyocytes upon exposure to hypoxia/reoxygenation (H/R) damage has not yet been elucidated. The present study aimed to investigate the potential protective role and underlying mechanisms of IL-35 in H/R-induced mouse neonatal cardiomyocyte injury. Mouse neonatal cardiomyocytes were challenged to H/R in the presence of IL-35, and we found that IL-35 dose dependently promotes cell viability, diminishes mtROS, maintains mitochondrial membrane potential, and decreases the number of apoptotic cardiomyocytes. Meanwhile, IL-35 remarkably activates mitochondrial STAT3 (mitoSTAT3) signaling, inhibits cytochrome c release, and reduces apoptosis signaling. Furthermore, co-treatment of the cardiomyocytes with the STAT3 inhibitor AG490 abrogates the IL-35-induced cardioprotective effects. Our study identified the protective role of IL-35 in cardiomyocytes following H/R damage and revealed that IL-35 protects cardiomyocytes against mtROS-induced apoptosis through the mitoSTAT3 signaling pathway during H/R."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.org/dc/terms/identifier | "doi:10.1093/abbs/gmab007"xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Feng T."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Lu X."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Zhang Q."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Zhang X."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Wang H."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Zhou F."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/author | "Xiu J."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/name | "Acta Biochim Biophys Sin (Shanghai)"xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/pages | "410-418"xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/title | "Interleukin 35 protects cardiomyocytes following ischemia/reperfusion-induced apoptosis via activation of mitochondrial STAT3."xsd:string |
http://purl.uniprot.org/citations/33619515 | http://purl.uniprot.org/core/volume | "53"xsd:string |
http://purl.uniprot.org/citations/33619515 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/33619515 |
http://purl.uniprot.org/citations/33619515 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/33619515 |
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http://purl.uniprot.org/uniprot/#_P42227-mappedCitation-33619515 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33619515 |
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http://purl.uniprot.org/uniprot/#_Q3U5Q4-mappedCitation-33619515 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33619515 |
http://purl.uniprot.org/uniprot/#_Q99ML3-mappedCitation-33619515 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33619515 |
http://purl.uniprot.org/uniprot/#_Q8CFJ6-mappedCitation-33619515 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33619515 |