LATS2 Deletion Attenuates Myocardial Ischemia-Reperfusion Injury by Promoting Mitochondrial Biogenesis.

Tytuł:: LATS2 Deletion Attenuates Myocardial Ischemia-Reperfusion Injury by Promoting Mitochondrial Biogenesis.
Autorzy:: Chen Y; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Liu C; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Li J; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Zhou P; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Zhao X; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Chen R; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Song L; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Zhao H; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.; Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, China.
Yan H; Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.; Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, China.
Źródło:: Oxidative medicine and cellular longevity [Oxid Med Cell Longev] 2021 Aug 17; Vol. 2021, pp. 1058872. Date of Electronic Publication: 2021 Aug 17 (Print Publication: 2021).
Typ publikacji:: Journal Article; Retracted Publication
Język:: English
Imprint Name(s):: Publication: 2011- : New York : Hindawi Pub. Corp.
Original Publication: 2008-2010: Austin, TX : Landes Bioscience
MeSH Terms:: Membrane Potential, Mitochondrial*
Organelle Biogenesis*
Myocardial Reperfusion Injury/*prevention & control
Myocytes, Cardiac/*cytology
Protein Serine-Threonine Kinases/*deficiency
Animals ; Cells, Cultured ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Myocytes, Cardiac/metabolism ; Rats
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Substance Nomenclature:: EC 2.7.11.1 (Lats2 protein, rat)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
Entry Date(s):: Date Created: 20210830 Date Completed: 20210913 Latest Revision: 20230202
Update Code:: 20240105
PubMed Central ID:: PMC8390173
DOI:: 10.1155/2021/1058872
PMID:: 34457109
: Czasopismo naukowe

Reperfusion therapy is the most effective treatment for acute myocardial infarction, but it can damage cardiomyocytes through a mechanism known as myocardial ischemia/reperfusion injury (MIRI). In this study, we investigated whether the large tumor suppressor kinase 2 (LATS2) contributes to the development of myocardial MIRI by disrupting mitochondrial biogenesis. Our in vitro data demonstrate that cardiomyocyte viability was reduced and apoptosis was increased in response to hypoxia/reoxygenation (H/R) injury. However, suppression of LATS2 by shRNA sustained cardiomyocyte viability by maintaining mitochondrial function. Compared to H/R-treated control cardiomyocytes, cardiomyocytes transfected with LATS2 shRNA exhibited increased mitochondrial respiration, improved mitochondrial ATP generation, and more stable mitochondrial membrane potential. LATS2 suppression increased cardiomyocyte viability and mitochondrial biogenesis in a manner dependent on PGC1 α , a key regulator of mitochondrial metabolism. These results identify LATS2 as a new inducer of mitochondrial damage and myocardial MIRI and suggest that approaches targeting LATS2 or mitochondrial biogenesis may be beneficial in the clinical management of cardiac MIRI.
Competing Interests: There is no conflict of interest in this study.
(Copyright © 2021 Yi Chen et al.)

Retraction in: Oxid Med Cell Longev. 2023 Jan 23;2023:9763942. (PMID: 36726360)

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