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Deficit of female sex hormones desensitizes rat cardiac mitophagy
Author(s) -
Theerachat Kampaengsri,
Marisa Ponpuak,
Jonggonnee Wattanapermpool,
Tepmanas Bupha-Intr
Publication year - 2021
Publication title -
chinese journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.396
H-Index - 31
eISSN - 2666-0059
pISSN - 0304-4920
DOI - 10.4103/cjp.cjp_102_20
Subject(s) - mitophagy , autophagy , endocrinology , mitochondrion , hormone , medicine , ovariectomized rat , parkin , cardiomyopathy , biology , cardiolipin , microbiology and biotechnology , heart failure , apoptosis , phospholipid , biochemistry , disease , membrane , parkinson's disease
Long-term deprivation of female sex hormones has been shown to mediate accumulation of damaged mitochondria in ventricular muscle leading to cardiovascular dysfunction. Therefore, the roles of female sex hormones in mitochondrial quality control are closely focused. In the present study, depletion of female sex hormones impairing mitochondrial autophagy in the heart was hypothesized. Cardiac mitophagy was therefore investigated in the heart of 10-week ovariectomized (OVX) and sham-operated (SHAM) rats. By using isolated mitochondria preparation, results demonstrated an increase in mitochondrial PTEN-induced kinase 1 accumulation in the sample of OVX rats indicating mitochondrial outer membrane dysfunction. However, no change in p62 and LC3-II translocation to mitochondria was observed between two groups indicating unresponsiveness of mitophagosome formation in the OVX rat heart. This loss might be resulted from significant decreases in Parkin and Bcl2l13 expression, but not Bnip3 activation. In summary, results suggest that mitochondrial abnormality in the heart after deprivation of female sex hormones could consequently be due to desensitization of mitophagy process.

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