Cell death-inducing DNA fragmentation factor alpha-like effector A (CIDEA)

Cell death-inducing DNA fragmentation factor alpha-like effector A (CIDEA) is a member of the CIDE family of proteins, primarily recognized for its critical role in regulating lipid metabolism and energy homeostasis [1, 2]. It is highly expressed in brown adipose tissue and, to a lesser extent, in white adipose tissue and the liver [1]. CIDEA localizes to the surface of lipid droplets, where it promotes their fusion and enlargement, thereby facilitating efficient lipid storage [4]. Additionally, CIDEA interacts with uncoupling protein 1 (UCP1) in the mitochondria of brown adipocytes, where it acts as a negative regulator of thermogenesis to conserve energy [3]. In humans, CIDEA expression levels in white adipose tissue are strongly correlated with metabolic health, often showing altered expression in individuals with obesity or type 2 diabetes [5]. Research suggests that inhibiting CIDEA could be a viable therapeutic strategy for treating metabolic disorders, as CIDEA-deficient models exhibit increased metabolic rate, resistance to diet-induced obesity, and improved insulin sensitivity [3]. While no clinical drugs currently target CIDEA directly, it remains a significant focus for the development of anti-obesity therapies, including antisense oligonucleotides and small molecule inhibitors [5].

Other names

CIDE-ACell death-inducing DFFA-like effector A

Modulation of lipid droplet fusion and suppression of uncoupling protein 1 (UCP1) activity to regulate energy expenditure and lipid storage.