Objective 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 Adult male C57BL / 6J mice (5 months old) and early-aging mice (21 months old) ( n= 9 per group) were housed in a specific-pathogen-free environment. Cardiac tissues were collected for micro-computed tomography scanning. Paraffin-embedded sections were stained with hematoxylin / eosin and Van Gieson stain. Cardiac mitochondria were extracted to measure reactive oxygen species (ROS) and expression levels of the dynamics-related proteins dynamin-related protein 1 ( Drp1), mitofusin 2 ( Mfn2), and optic atrophy 1 ( OPA1). Mitochondrial ultrastructure was observed using transmission electron microscopy. Protein expression levels of the inflammatory markers receptor-interacting serine / threonine-protein kinase 3 ( RIP3) and phosphorylated nuclear factor ( p-NF- κB), the fibrosis marker Bcl-2-associated X protein( Bax),collagen type I, the apoptosis markers caspase-3 and cleaved caspase-3, the autophagy markers phosphorylated protein kinase B (p-Akt), protein kinase B (Akt), and microtubule-associated protein 1 light chain 3 I/ II (LC3I/ II), and the ferroptosis markers acyl-CoA synthetase longchain family member 4 (ACSL4) and solute carrier family 7 member 11 (SLC7A11) were measured by Western blot. Results Compared with adult mice, early-aged mice exhibited myocardial hypertrophy and fibrosis, disordered cardiomyocyte arrangement, and increased mitochondrial ROS levels (P<0. 05). There was no significant change in expression levels of the mitochondrial fission-related protein Drp1, but expression levels of the fusion-related proteins Mfn2 and OPA1 were increased (P<0. 05). Electron microscopy revealed swelling and disordered cristae structures in myocardial mitochondria. Expression levels of the myocardial fibrosis marker Collagen I(P<0. 01), as well as the inflammation-related markers RIP3 and p-NF-κB, were elevated ( P<0. 01). In contrast, expression levels of the autophagy-related protein LC3II were reduced (P<0. 05), while the expression of Bax was increased (P<0. 01),with no significant change in expression of the apoptosis-related protein Cleaved Caspase-3. In addition, expression of the ferroptosis-related protein ACSL4 was increased ( P<0. 001), whereas SLC7A11 expression was decreased ( P<0. 05). Conclusions Early cardiac aging is characterized by hypertrophy and myocardial fibrosis, accompanied by inflammation, mitochondrial dysfunction, and dynamics imbalance. Notably, ferroptosis, rather than apoptosis, emerges as the primary pathway of programmed cell death during the early stages of cardiac aging.