Prkg1, also known as cGMP-dependent protein kinase I, is a crucial gene involved in multiple biological processes. It is part of the cGMP-Prkg1 signaling pathway, which plays significant roles in various physiological functions [1,3,4]. For example, it is involved in processes like regulating mitochondrial function, synaptic transmission, and smooth muscle motility, highlighting its overall biological importance. Genetic models, such as KO/CKO mouse models, can be valuable for studying its functions.

In a DIC mouse model, vericiguat was found to improve mitochondrial dysfunction and reduce mtDNA leakage by up-regulating Prkg1, which then activated PINK1 and inhibited the STING/IRF3 pathway to alleviate DIC, suggesting Prkg1's role in cardiac protection [1]. In mice, DMH-specific Prkg1 knockdown suppressed age-associated Ppp1r17 translocation, ameliorated age-associated dysfunction in WAT, increased physical activity, and extended lifespan, indicating Prkg1's involvement in regulating aging [2]. In noise-induced hearing loss (NIHL) mouse models, genetic deletion of Prkg1 led to greater vulnerability and less recovery from NIHL, suggesting its role in protecting cochlear hair cells and hearing function [4].

In conclusion, Prkg1 is essential in regulating mitochondrial function, aging-related processes, and hearing protection. The use of Prkg1 KO/CKO mouse models has significantly contributed to understanding its role in diseases such as doxorubicin-induced cardiotoxicity and NIHL, providing insights into potential therapeutic targets for these conditions.