**Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts**

**Mi-Hyun No 1 , Youngju Choi 2 , Jinkyung Cho 2 , Jun-Won Heo 1,2 , Eun-Jeong Cho 1,2 , Dong-Ho Park 1,2 , Ju-Hee Kang 2,3 , Chang-Ju Kim <sup>4</sup> , Dae Yun Seo 5 , Jin Han <sup>5</sup> and Hyo-Bum Kwak 1,2, \***


Received: 20 July 2020; Accepted: 4 September 2020; Published: 5 September 2020

**Abstract:** 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.

**Keywords:** aging heart; Bcl-2 family; mitochondria; programmed cell death
