Unknown

Dataset Information

0

Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts.


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.

SUBMITTER: No MH 

PROVIDER: S-EPMC7555313 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

altmetric image

Publications


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 Fisc  ...[more]

Similar Datasets

| S-EPMC3268156 | biostudies-literature
| S-EPMC4914251 | biostudies-literature
| S-EPMC6128413 | biostudies-literature
| S-EPMC7893175 | biostudies-literature
| S-EPMC4571548 | biostudies-literature
| S-EPMC549619 | biostudies-literature
| S-EPMC3734287 | biostudies-literature
| S-EPMC2685531 | biostudies-literature
2021-06-18 | PXD026773 | Pride
| S-EPMC7007135 | biostudies-literature