http://purl.uniprot.org/citations/37497006 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/37497006 | http://www.w3.org/2000/01/rdf-schema#comment | "Large tumor suppressor kinase 2 (Lats2) is a member of the Hippo pathway, a critical regulator of organ size. Since Lats2 activity may trigger mitochondrial dysfunction, a key pathogenic factor in acute myocardial infarction (AMI), this study sought to investigate whether Lats2 deletion confers cardioprotection in AMI. AMI was induced in cardiomyocyte-specific Lats2 knockout (Lats2Cko) and control (Lats2flox) mice. Twenty-eight days after AMI surgery, myocardial performance and mitochondrial homeostasis were impaired in Lats2floxmice. In contrast, Lats2Cko mice exhibited markedly preserved cardiac structure and contraction/relaxation activity, decreased fibrosis, reduced circulating cardiac injury biomarker levels, and enhanced cardiomyocyte viability. Consistent with these findings, siRNA-mediated Lats2 silencing sustained mitochondrial respiration and inhibited apoptosis in hypoxia-treated HL-1 cardiomyocytes. Notably, Lats2 deficiency inhibited AMI/hypoxia-related mitochondrial fission and inactivated STING/p65 signaling by preventing hypoxia-induced release of mtDNA into the cytosol. Accordingly, pharmacological reactivation of STING signaling abolished the cardioprotective effects of Lats2 ablation. Those data suggest that AMI-induced Lats2 upregulation is associated with impaired cardiomyocyte viability and function resulting from enhanced mitochondrial fission, mtDNA release, and STING/p65 pathway activation."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.org/dc/terms/identifier | "doi:10.7150/ijbs.84426"xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/author | "Du Y."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/author | "He J."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/author | "Huang S."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/author | "Liu L."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/author | "Zhou H."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/author | "Zhang K."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/name | "Int J Biol Sci"xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/pages | "3428-3440"xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/title | "Lats2 deficiency protects the heart against myocardial infarction by reducing inflammation and inhibiting mitochondrial fission and STING/p65 signaling."xsd:string |
http://purl.uniprot.org/citations/37497006 | http://purl.uniprot.org/core/volume | "19"xsd:string |
http://purl.uniprot.org/citations/37497006 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/37497006 |
http://purl.uniprot.org/citations/37497006 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/37497006 |
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http://purl.uniprot.org/uniprot/#_A0A2U8RP79-mappedCitation-37497006 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37497006 |
http://purl.uniprot.org/uniprot/#_A0A494B9A3-mappedCitation-37497006 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37497006 |
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