Transcriptional cyclin-dependent kinases as the mediators of inflammation-a review.

Cyclin-dependent kinases (CDKs) belong to the serine/threonine kinase family, and their unique interactions with a variety of cyclin complexes influence its catalytic activity to ensure unimpaired cell cycle progression. In addition to their cell cycle regulatory roles, it is becoming increasingly clear that the CDKs can have multiple functional roles like transcription, epigenetic regulation, metabolism, stem cell self-renewal, neuronal functions, and in spermatogenesis. Further in addition, recent reports suggest that CDKs have a remarkable regulatory role in influencing the pro-inflammatory functions of various cytokines during the clinical inflammatory responses. CDKs initiate the inflammatory responses by triggering the activity of prominent pro-inflammatory transcription factors such as nuclear factor kappa B (NF-kB), signal transducer and activator of transcription 3 (STAT3), and activator protein 1 (AP-1). The transcriptional CDKs (tCDKs) is crucial for organizing various transcription events and associated processes such as RNA capping, splicing, 3' end formation, and chromatin remodeling. Although the in-depth mechanism of certain mammalian CDKs is explored with respect to inflammation, the role of other tCDKs or any synergistic play among the members still remains unexplored. Until today, there is only supportive and palliative care available most of the inflammatory disorders, and thus it is the right time to explore novel pharmacological targets. In this regard, we focus on the pathophysiological role of CDK7, CDK8 and CDK9 and their impact on the development of inflammatory disorders within the mammals. Additionally, we discuss the potential trends of having tCDKs as a therapeutic target for fine-tuning inflammatory disorders.