Tubular deletion of CPT1A minimally affects aging and chronic kidney injury. This study investigated the role of tubular CPT1A in aging and injury by generating mice with tubule-specific deletion of Cpt1a (Cpt1aCKO mice). These mice were either aged for 2 years or subjected to chronic injury models, including aristolochic acid nephropathy (AAN) and unilateral ureteral obstruction (UUO). Despite the deletion of Cpt1a, there were no significant differences in kidney function or fibrosis compared to wild-type mice after aging or chronic injury. Primary tubule cells from aged Cpt1aCKO mice had a modest decrease in palmitate oxidation but retained the ability to metabolize long-chain fatty acids. Very-long-chain fatty acids, exclusively oxidized by peroxisomes, were reduced in kidneys lacking tubular CPT1A, consistent with increased peroxisomal activity. Single-nuclear RNA-Seq showed significantly increased expression of peroxisomal FAO enzymes in proximal tubules of mice lacking tubular CPT1A. These data suggest that peroxisomal FAO may compensate in the absence of CPT1A, and future genetic studies are needed to confirm the role of peroxisomal β-oxidation when mitochondrial FAO is impaired. The kidney is a highly metabolically active organ, primarily due to the energy demands of the proximal tubules. The large water and solute reabsorptive capacity of proximal tubules necessitates high rates of ATP production. Thus, proximal tubules have large amounts of mitochondria to generate ATP and preferentially use fatty acid oxidation (FAO), which produces more ATP than glucose, as their preferred energy substrate. Impaired FAO has been described in both acute and chronic kidney injury. Reduced FAO not only reflects kidney injury, but also is thought to play an important role in the pathogenesis of kidney injury through diminished ATP, accumulation of intracellular lipids, and reduced mitochondrial function. These effects all promote tubular atrophy and tubulointerstitial fibrosis, the hallmarks of chronic kidney disease (CKD) progression. The aging kidney shares many features of CKD, including glomerulosclerosis, tubulointerstitial fibrosis, and tubular atrophy. The pathophysiology of age-associated renal fibrosis is multifactorial and includes the progressive loss of nephrons, cell senescence, inflammation, and dysfunctional mitochondria with ROS production. Altered metabolism may also play a role in aging-mediated pathological changes in the kidney, as proteins involved in FAO were decreased in the aged rat kidney. PPARα transcriptionally upregulates many genes involved in FAO, and aged Ppara−/− mice had worsened kidney fibrosis, suggesting that reduced FAO may be linked mechanistically to aged-induced renal fibrosis. CarnTubular deletion of CPT1A minimally affects aging and chronic kidney injury. This study investigated the role of tubular CPT1A in aging and injury by generating mice with tubule-specific deletion of Cpt1a (Cpt1aCKO mice). These mice were either aged for 2 years or subjected to chronic injury models, including aristolochic acid nephropathy (AAN) and unilateral ureteral obstruction (UUO). Despite the deletion of Cpt1a, there were no significant differences in kidney function or fibrosis compared to wild-type mice after aging or chronic injury. Primary tubule cells from aged Cpt1aCKO mice had a modest decrease in palmitate oxidation but retained the ability to metabolize long-chain fatty acids. Very-long-chain fatty acids, exclusively oxidized by peroxisomes, were reduced in kidneys lacking tubular CPT1A, consistent with increased peroxisomal activity. Single-nuclear RNA-Seq showed significantly increased expression of peroxisomal FAO enzymes in proximal tubules of mice lacking tubular CPT1A. These data suggest that peroxisomal FAO may compensate in the absence of CPT1A, and future genetic studies are needed to confirm the role of peroxisomal β-oxidation when mitochondrial FAO is impaired. The kidney is a highly metabolically active organ, primarily due to the energy demands of the proximal tubules. The large water and solute reabsorptive capacity of proximal tubules necessitates high rates of ATP production. Thus, proximal tubules have large amounts of mitochondria to generate ATP and preferentially use fatty acid oxidation (FAO), which produces more ATP than glucose, as their preferred energy substrate. Impaired FAO has been described in both acute and chronic kidney injury. Reduced FAO not only reflects kidney injury, but also is thought to play an important role in the pathogenesis of kidney injury through diminished ATP, accumulation of intracellular lipids, and reduced mitochondrial function. These effects all promote tubular atrophy and tubulointerstitial fibrosis, the hallmarks of chronic kidney disease (CKD) progression. The aging kidney shares many features of CKD, including glomerulosclerosis, tubulointerstitial fibrosis, and tubular atrophy. The pathophysiology of age-associated renal fibrosis is multifactorial and includes the progressive loss of nephrons, cell senescence, inflammation, and dysfunctional mitochondria with ROS production. Altered metabolism may also play a role in aging-mediated pathological changes in the kidney, as proteins involved in FAO were decreased in the aged rat kidney. PPARα transcriptionally upregulates many genes involved in FAO, and aged Ppara−/− mice had worsened kidney fibrosis, suggesting that reduced FAO may be linked mechanistically to aged-induced renal fibrosis. Carn