Ciart-flox Mouse

Ciart, the circadian-associated repressor of transcription, is involved in the regulation of circadian rhythms, which are crucial for proper behavioral, physiological, and molecular functions in the body [2,3,4,7,9]. It is associated with multiple pathways, and its dysregulation may impact various biological processes [3,4,9]. Genetic models, such as gene knockout models, can be valuable for studying its functions.

Lung airway organoids, lung alveolar organoids, and cardiomyocytes derived from isogenic CIART-/-human pluripotent stem cells were significantly resistant to SARS-CoV-2 infection, suggesting that Ciart is a key factor for SARS-CoV-2 infection, potentially through regulating NR4A1 and the Retinoid X Receptor pathway [1]. In spinal cord injury-induced immunodeficiency, upregulated genes in the adrenal glands including Ciart were enriched in cortisol secretion and circadian rhythm changes [3]. In hypertensive rats, ARB-modified gut microbiota increased intestinal Ciart levels, which was linked to protective effects against hypertensive damages [4]. In crizotinib-induced cardiotoxicity in mice, Ciart was among the differentially expressed genes [5]. In the aging mouse lens, swimming exercise affected the expression of Ciart, with its protein-protein interaction network involving the regulation of Rorb and Sptbn5 [6]. In opioid-induced hyperalgesia, alternative splicing of Ciart was detected in the trigeminal ganglia of mice [8]. In a rat stress myocardial injury model, Ciart was significantly downregulated during water immersion stress, and melatonin's protective effect may be related to regulating Ciart expression [9].

In conclusion, Ciart plays essential roles in multiple biological processes, including virus infection, cortisol secretion, circadian rhythm, and tissue-specific responses to various stresses. Studies using gene knockout or related models have provided insights into its functions in diseases such as COVID-19, spinal cord injury-induced immunodeficiency, hypertension, cardiotoxicity, lens aging, opioid-induced hyperalgesia, and stress myocardial injury, helping to understand disease mechanisms and potentially identify therapeutic targets.