{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Myung J"],"funding":["faculty research grant from Yonsei University College of Medicine","National Research Foundation of Korea"],"pagination":["894"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9032004"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(4)"],"pubmed_abstract":["Currently, no effective therapy and potential target have been elucidated for preventing myocardial ischemia and reperfusion injury (I/R). We hypothesized that the administration of recombinant klotho (rKL) protein could attenuate the sterile inflammation in peri-infarct regions by inhibiting the extracellular release of high mobility group box-1 (HMGB1). This hypothesis was examined using a rat coronary artery ligation model. Rats were divided into sham, sham+ rKL, I/R, and I/R+ rKL groups (<i>n</i> = 5/group). Administration of rKL protein reduced infarct volume and attenuated extracellular release of HMGB1 from peri-infarct tissue after myocardial I/R injury. The administration of rKL protein inhibited the expression of pro-inflammatory cytokines in the peri-infarct regions and significantly attenuated apoptosis and production of intracellular reactive oxygen species by myocardial I/R injury. Klotho treatment significantly reduced the increase in the levels of circulating HMGB1 in blood at 4 h after myocardial ischemia. rKL regulated the levels of inflammation-related proteins. This is the first study to suggest that exogenous administration of rKL exerts myocardial protection effects after I/R injury and provides new mechanistic insights into rKL that can provide the theoretical basis for clinical application of new adjunctive modality for critical care of acute myocardial infarction."],"journal":["Biomedicines"],"pubmed_title":["Recombinant Klotho Protein Ameliorates Myocardial Ischemia/Reperfusion Injury by Attenuating Sterile Inflammation."],"pmcid":["PMC9032004"],"funding_grant_id":["NRF- 2018R1C1B6006159","NRF-2018R1D1A1B07044998","6-2020-0086","NRF-2021R1C1C1009209","NRF - 2019R1C1C1006332"],"pubmed_authors":["Myung J","Park I","Woo JS","Chung YE","Kim JH","You JS","Beom JH","Chung SP"],"additional_accession":[]},"is_claimable":false,"name":"Recombinant Klotho Protein Ameliorates Myocardial Ischemia/Reperfusion Injury by Attenuating Sterile Inflammation.","description":"Currently, no effective therapy and potential target have been elucidated for preventing myocardial ischemia and reperfusion injury (I/R). We hypothesized that the administration of recombinant klotho (rKL) protein could attenuate the sterile inflammation in peri-infarct regions by inhibiting the extracellular release of high mobility group box-1 (HMGB1). This hypothesis was examined using a rat coronary artery ligation model. Rats were divided into sham, sham+ rKL, I/R, and I/R+ rKL groups (<i>n</i> = 5/group). Administration of rKL protein reduced infarct volume and attenuated extracellular release of HMGB1 from peri-infarct tissue after myocardial I/R injury. The administration of rKL protein inhibited the expression of pro-inflammatory cytokines in the peri-infarct regions and significantly attenuated apoptosis and production of intracellular reactive oxygen species by myocardial I/R injury. Klotho treatment significantly reduced the increase in the levels of circulating HMGB1 in blood at 4 h after myocardial ischemia. rKL regulated the levels of inflammation-related proteins. This is the first study to suggest that exogenous administration of rKL exerts myocardial protection effects after I/R injury and provides new mechanistic insights into rKL that can provide the theoretical basis for clinical application of new adjunctive modality for critical care of acute myocardial infarction.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2025-04-04T07:45:56.39Z","creation":"2025-04-04T07:45:56.39Z"},"accession":"S-EPMC9032004","cross_references":{"pubmed":["35453645"],"doi":["10.3390/biomedicines10040894"]}}