Pex11a, peroxisomal biogenesis factor 11a, is crucial for peroxisome abundance and function. Peroxisomes play a central role in lipid metabolism, and Pex11a is involved in pathways related to fatty acid β -oxidation. Its proper function is essential for normal cellular metabolism and physiological processes [1,2,3]. Genetic models, such as knockout mice, are valuable for studying Pex11a's function.

In Pex11a knockout mice (Pex11a -/-), there are significant metabolic disruptions. These mice show increased fat mass, decreased skeletal muscle, higher cholesterol levels, and impaired glucose and insulin tolerance. They also consume less oxygen, indicating decreased fatty acid oxidation, along with the accumulation of very long-and long-chain fatty acids. In adipose tissue, palmitic acid levels are elevated, likely due to increased fatty acid synthase expression. Additionally, Pex11a deficiency leads to an enlarged ventricle, macrophage infiltration, and reduced physical activity [1]. In the kidney, Pex11a -/- mice have a reduced number of functional peroxisomes in proximal tubule cells, which aggravates tubulointerstitial lesions in chronic kidney disease models [2].

In conclusion, Pex11a is essential for maintaining normal lipid metabolism, physical activity, and energy expenditure. Pex11a knockout mouse models have revealed its role in dyslipidaemia, obesity, and chronic kidney disease, providing insights into the underlying molecular mechanisms and potential therapeutic targets for these conditions.