Cpt1c, a unique isoform of carnitine palmitoyltransferase, is pivotal in regulating fatty acid oxidation. It is involved in lipid metabolic reprogramming and cell adaptation to environmental stressors, rather than being a direct fat burner [2]. Cpt1c is expressed in various tissues, including neurons and is associated with multiple biological processes and diseases.

In gastric cancer, Cpt1c-positive cancer-associated fibroblasts (Cpt1c + CAFs) foster an immunosuppressive tumor microenvironment by promoting the IL-6-induced M2-like phenotype of macrophages, and are associated with therapeutic resistance [1]. In breast cancer, Cpt1c downregulation causes plasma membrane remodelling and anthracycline resistance [3]. In colorectal cancer, Cpt1c-mediated fatty acid oxidation facilitates cell proliferation and metastasis, and its overexpression indicates poor relapse-free survival [4]. In pancreatic cancer, the YY1-Cpt1c signaling axis modulates cell proliferation and metabolism under hypoxia [5]. In esophageal squamous cell carcinoma, Cpt1c promotes tumor progression by upregulating energy supply and accelerating the G1/S transition [6]. In the hypothalamus, Cpt1c in the ventromedial nucleus is necessary for brown fat thermogenesis activation in obesity [7].

In conclusion, Cpt1c plays diverse and significant roles in multiple biological processes and disease conditions, especially in cancer progression, energy homeostasis, and immune regulation. Studies on Cpt1c using gene knockout models in mice have provided valuable insights into its functions in these areas, helping to better understand the underlying mechanisms and potentially guiding the development of therapeutic strategies.