Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts
Mi-Hyun No,
Youngju Choi,
Jinkyung Cho,
Jun-Won Heo,
Eun-Jeong Cho,
Dong-Ho Park,
Ju-Hee Kang,
Chang-Ju Kim,
Dae Yun Seo,
Jin Han,
Hyo-Bum Kwak
Affiliations
Mi-Hyun No
Department of Biomedical Science, Program in Biomedical Science & Engineering, Department of Kinesiology, Inha University, Incheon 22212, Korea
Youngju Choi
Institute of Sports and Arts Convergence, Inha University, Incheon 22212, Korea
Jinkyung Cho
Institute of Sports and Arts Convergence, Inha University, Incheon 22212, Korea
Jun-Won Heo
Department of Biomedical Science, Program in Biomedical Science & Engineering, Department of Kinesiology, Inha University, Incheon 22212, Korea
Eun-Jeong Cho
Department of Biomedical Science, Program in Biomedical Science & Engineering, Department of Kinesiology, Inha University, Incheon 22212, Korea
Dong-Ho Park
Department of Biomedical Science, Program in Biomedical Science & Engineering, Department of Kinesiology, Inha University, Incheon 22212, Korea
Ju-Hee Kang
Institute of Sports and Arts Convergence, Inha University, Incheon 22212, Korea
Chang-Ju Kim
Department of Physiology, College of Medicine, Kyung Hee University, Seoul 02447, Korea
Dae Yun Seo
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea
Jin Han
National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea
Hyo-Bum Kwak
Department of Biomedical Science, Program in Biomedical Science & Engineering, Department of Kinesiology, Inha University, Incheon 22212, Korea
Aging represents a major risk for developing cardiac disease, including heart failure. The gradual deterioration of cell quality control with aging leads to cell death, a phenomenon associated with mitochondrial dysfunction in the heart. Apoptosis is an important quality control process and a necessary phenomenon for maintaining homeostasis and normal function of the heart. However, the mechanism of mitochondria-mediated apoptosis in aged hearts remains poorly understood. Here, we used male Fischer 344 rats of various ages, representing very young (1 month), young (4 months), middle-aged (12 months), and old (20 months) rats, to determine whether mitochondria-mediated apoptotic signals and apoptosis in the left ventricle of the heart are altered notably with aging. As the rats aged, the extramyocyte space and myocyte cross-sectional area in their left ventricle muscle increased, while the number of myocytes decreased. Additionally, mitochondrion-mediated apoptotic signals and apoptosis increased remarkably during aging. Therefore, our results demonstrate that aging promotes remarkable morphological changes and increases the degree of mitochondrion-mediated apoptosis in the left ventricle of rat hearts.
