Objective This study aims to preliminarily explore the role of mitochondria-related programmed cell death mechanisms, including apoptosis, autophagy, and ferroptosis, in early aging cardiac hypertrophy and myocardial fibrosis. Methods Male young C57BL/6 mice (5 months old, n=6) and early aging mice (21 months old, n=6) were housed in a specific pathogen-free (SPF) environment. Cardiac tissues were collected for micro-CT scanning imaging. Paraffin sections were subjected to H E and Van Gieson staining. Cardiac mitochondria were extracted to measure reactive oxygen species (ROS) levels and the expression of dynamics-related proteins dynamin-related protein 1 (Drp1), mitofusin 2 (Mfn2), and optic Atrophy 1 (OPA1). The ultrastructure of mitochondria was observed using transmission electron microscopy. Western blot analysis was performed to assess the protein expression levels of inflammatory markers receptor-interacting serine/threonine-protein kinase 3 (RIP3) and phosphorylated Nuclear Factor kappa B (p-NF-κB), fibrosis marker collagen type I (Collagen I), apoptosis markers cysteinyl aspartatespecific protease-3 (Caspase-3) and cleaved cysteinyl aspartatespecific protease-3 (Cleaved caspase-3), autophagy markers phosphorylated protein kinase B (p-Akt), protein kinase B (Akt), and microtubule-associated protein 1 light chain 3 I/II (LC3I/II), as well as ferroptosis markers acyl-coa synthetase long-chain family member 4 (ACSL4) and solute carrier family 7 member 11 (SLC7A11). Results Compared with young mice, early-aged mice exhibited myocardial hypertrophy and fibrosis, disordered cardiomyocyte arrangement, increased mitochondrial ROS levels, and no significant changes in the expression of the mitochondrial fission-related protein Drp1. However, there was an increased expression of the fusion-related proteins Mfn2 and OPA1. Electron microscopy revealed that myocardial mitochondria displayed swelling and disordered cristae structures. The expression of the myocardial fibrosis marker Collagen I was found to be elevated, alongside an increase in the inflammation-related markers RIP3 and p-NF-κB. In contrast, the expression of the autophagy-related protein LC3 II was reduced, while no significant change was observed in the expression of the apoptosis-related protein cleaved caspase-3. Additionally, the expression of the ferroptosis-related protein ACSL4 was increased, whereas the expression of SLC7A11 was decreased. Conclusion Early cardiac aging is characterized by hypertrophy and myocardial fibrosis, which are accompanied by inflammation, mitochondrial dysfunction, and kinetic imbalance. Notably, ferroptosis, rather than apoptosis, emerges as the primary pathway of programmed cell death during the early stages of cardiac aging.