Carmn, short for cardiac mesoderm enhancer-associated noncoding RNA, is a long noncoding RNA. It is crucial for maintaining the contractile phenotype of smooth muscle cells (SMCs) by binding to myocardin, a key transcriptional cofactor. This function is vital for vascular homeostasis, as well as for the proper function of the gastrointestinal tract [1,3]. It may also be involved in the regulation of gene expression and cellular processes related to various diseases, potentially through associated pathways like Wnt/β-catenin in cervical cancer [2]. Genetic models, such as the Carmn green fluorescent protein knock-in reporter mouse model, are valuable for studying Carmn [1].

SMC-specific deletion of Carmn in mice significantly exacerbated injury-induced neointima formation, indicating its role in vascular diseases [1]. In Carmn knockout (KO) mice, premature lethality occurred due to gastrointestinal pseudo-obstruction, severe distension of the GI tract, and dysmotility in the cecum and colon segments. Loss of Carmn promoted SMC phenotypic switching, up-regulating extracellular matrix genes and down-regulating SMC contractile genes [3].

In conclusion, Carmn is essential for maintaining the contractile function of SMCs in both vascular and gastrointestinal systems. Studies using Carmn KO mouse models have revealed its significance in vascular diseases and visceral myopathy, highlighting its potential as a therapeutic target in these disease areas.