Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses

Cardiovascular Research
Toshiro SaitoDongchon Kang

Abstract

Mitochondria are important organelles, dedicated to energy production. Mitochondrial p32/C1qbp, which functions as an RNA and protein chaperone, interacts with mitochondrial mRNA and is indispensable for mitochondrial function through its regulation of mitochondrial translation in cultured cell lines. However, the precise role of p32/C1qbp in vivo is poorly understood because of embryonic lethality in the systemic p32-deficient mouse. The goal of this study was to examine the physiological function of mitochondrial p32/C1qbp in the heart. We investigated the role of p32 in regulating cardiac function in mice using a Cre-loxP recombinase technology against p32 with tamoxifen-inducible knockdown or genetic ablation during postnatal periods. Cardiomyocyte-specific deletion of p32 resulted in contractile dysfunction, cardiac dilatation and cardiac fibrosis, compared with hearts of control mice. We also found decreased COX1 expression, decreased rates of oxygen consumption and increased oxidative stress, indicating that these mice had cardiac mitochondrial dysfunction provoked by p32-deficiency at early stage. Next, we investigated lifespan in cardiac-specific p32-deficient mice. The mice died beginning at 12 months and their median...Continue Reading

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Citations

Oct 17, 2017·Cardiovascular Research·Maurilio Sampaolesi, Kristel Van Calsteren
Mar 18, 2020·Nucleic Acids Research·Sabrina SummerAlexandre Smirnov
Feb 3, 2021·The EMBO Journal·Mikako YagiTakeshi Uchiumi
Oct 17, 2020·Journal of Cardiothoracic Surgery·Toshiro SaitoKimikazu Hamano
May 19, 2021·American Journal of Medical Genetics. Part a·Gregory WebsterMegan J Puckelwartz
Aug 24, 2021·Frontiers in Immunology·Soichi MizuguchiDongchon Kang

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