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Lipogenic genes refer to a functional collective of enzymes and transcription factors that orchestrate de novo lipogenesis (DNL), the metabolic pathway responsible for converting excess carbon sources like carbohydrates into fatty acids. Key members of this group include ATP-citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), fatty acid synthase (FASN), and stearoyl-CoA desaturase-1 (SCD1), which are primarily regulated by the transcription factors SREBP-1c and ChREBP [6, 11]. In metabolic conditions such as metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity, these genes are pathologically upregulated, leading to excessive lipid accumulation in the liver and systemic lipotoxicity [1, 5]. Pharmacological inhibition of specific proteins within this group, such as FASN or ACC, is currently being investigated as a therapeutic strategy to reduce hepatic fat and inflammation [3, 4]. Furthermore, because rapidly proliferating cancer cells rely on these genes to supply fatty acids for new membrane synthesis, they are also considered viable targets in oncology [9, 10].
Inhibition of specific enzymatic steps within the lipogenic pathway (such as ACLY, ACC, or FASN) to block the synthesis of long-chain fatty acids from acetyl-CoA, thereby reducing cellular lipid stores and signaling lipids [6, 13].
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