Furihata 2021 Commun Biol
|Furihata T, Takada S, Kakutani N, Maekawa S, Tsuda M, Matsumoto J, Mizushima W, Fukushima A, Yokota T, Enzan N, Matsushima S, Handa H, Fumoto Y, Nio-Kobayashi J, Iwanaga T, Tanaka S, Tsutsui H, Sabe H, Kinugawa S (2021) Cardiac-specific loss of mitoNEET expression is linked with age-related heart failure. Commun Biol 4:138.|
Furihata Takaaki, Takada Shingo, Kakutani Naoya, Maekawa Satoshi, Tsuda Masaya, Matsumoto Junichi, Mizushima Wataru, Fukushima Arata, Yokota Takashi, Enzan Nobuyuki, Matsushima Shouji, Handa Haruka, Fumoto Yoshizuki, Nio-Kobayashi Junko, Iwanaga Toshihiko, Tanaka Shinya, Tsutsui Hiroyuki, Sabe Hisataka, Kinugawa Shintaro (2021) Commun Biol
Abstract: Heart failure (HF) occurs frequently among older individuals, and dysfunction of cardiac mitochondria is often observed. We here show the cardiac-specific downregulation of a certain mitochondrial component during the chronological aging of mice, which is detrimental to the heart. MitoNEET is a mitochondrial outer membrane protein, encoded by CDGSH iron sulfur domain 1 (CISD1). Expression of mitoNEET was specifically downregulated in the heart and kidney of chronologically aged mice. Mice with a constitutive cardiac-specific deletion of CISD1 on the C57BL/6J background showed cardiac dysfunction only after 12 months of age and developed HF after 16 months; whereas irregular morphology and higher levels of reactive oxygen species in their cardiac mitochondria were observed at earlier time points. Our results suggest a possible mechanism by which cardiac mitochondria may gradually lose their integrity during natural aging, and shed light on an uncharted molecular basis closely related to age-associated HF.
Labels: MiParea: Respiration, Genetic knockout;overexpression Pathology: Aging;senescence, Cardiovascular
Organism: Mouse Tissue;cell: Heart Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS, ET Pathway: N, S, NS, ROX HRR: Oxygraph-2k, O2k-Fluorometer
2021-02, AmR, JP