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, 3ʹ 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.

细胞周期蛋白依赖性激酶（CDK）属于丝氨酸/苏氨酸激酶家族，它们与多种细胞周期蛋白复合物的独特相互作用会影响其催化活性，从而确保细胞周期进程不受损害。除了它们的细胞周期调节作用外，越来越清楚的是CDK可以具有多种功能作用，例如转录，表观遗传调节，代谢，干细胞自我更新，神经元功能以及精子发生。另外，最近的报道表明，CDK在临床炎症反应过程中在影响各种细胞因子的促炎功能方面具有显着的调节作用。CDK通过触发突出的促炎性转录因子（例如核因子κB（NF-kB），信号转导子和转录激活子3（STAT3），以及激活蛋白1（AP-1）。转录CDK（tCDK）对于组织各种转录事件和相关过程（例如RNA封端，剪接，3′末端形成和染色质重塑）至关重要。尽管已就炎症方面探讨了某些哺乳动物CDK的深入机制，但其他tCDK的作用或成员之间的任何协同作用仍未探索。直到今天，大多数炎症性疾病都只有支持和姑息治疗，因此，现在是探索新药理学靶标的正确时机。在这方面，我们专注于CDK7，CDK8和CDK9的病理生理作用及其对哺乳动物体内炎症性疾病发展的影响。另外，