Current Drug Targets - Volume 25, Issue 13, 2024

An aneurysm is an abnormal enlargement or bulging of the wall of a blood vessel. Most often, aneurysms occur in large blood vessels - the aorta (Thoracic Aortic Aneurysm (TAA) and Abdominal Aortic Aneurysm (AAA)) and brain vessels (Intracranial Aneurysm (IA)). Despite the presence of significant differences in the pathogenesis of the development and progression of IA and TAA/AAA, there are also similarities. For instance, both have been shown to be strongly influenced by shear stress, inflammatory processes, and enzymatic destruction of the elastic lamellae and extracellular matrix (ECM) proteins of the vascular wall. Moreover, although IA and TAA are predominantly considered arteriopathies with different pathological mechanisms, they share risk factors with AAA, such as hypertension and smoking. However, there is a need for a more in-depth study of the key elements that may influence the formation and progression of a particular aneurysm to find ways of therapeutic intervention or search for a diagnostic tool. Today, it is known that the disruption of gene expression is one of the main mechanisms that contribute to the development of aneurysms. At the same time, growing evidence suggests that aberrant epigenetic regulation of gene function is strongly related to the genesis of aneurysms. Although much has been studied of the known protein-coding genes, circular RNAs (circRNAs), a relatively new and rapidly evolving large family of transcripts, have recently received much scientific attention. CircRNAs regulate gene expression through the sponging of microRNAs (miRNAs) and can also be used as therapeutic targets and biomarkers. Increasing evidence has implicated circRNAs in the pathogenesis of multiple cardiovascular diseases, including the development of aneurysms. However, the mechanism of dysregulation of certain circRNAs in a particular aneurysm remains to be studied. The discovery of circRNAs has recently advanced our understanding of the latest mode of miRNAs/target genes regulation in the development and progression of IA and TAA/AAA. The aim of this study is to compare the expression profiles of circRNAs to search for similar or different effects of certain circRNAs on the formation and progression of IA and TAA/AAA.

The global burden of neurological disorders is evident, yet there remains limited efficacious therapeutics for their treatment. There is a growing recognition of the role of inflammation in diseases of the central nervous system (CNS); among the numerous inflammatory mediators involved, prostaglandins play a crucial role. Prostaglandins are small lipid mediators derived from arachidonic acid via multi-enzymatic pathways. The actions of prostaglandins are varied, with each prostaglandin having a specific role in maintaining homeostasis. In the CNS, prostaglandins can have neuroprotective or neurotoxic properties depending on their specific G-protein receptor. These G-protein receptors have varying subfamilies, tissue distribution, and signal transduction cascades. Further studies into the impact of prostaglandins in CNS-based diseases may contribute to the clarification of their actions, hopefully leading to the development of efficacious therapeutic strategies. This review focuses on the roles played by prostaglandins in neural degeneration, with a focus on Alzheimer’s Disease, Multiple Sclerosis, and Amyotrophic Lateral Sclerosis in both preclinical and clinical settings. We further discuss current prostaglandin-related agonists and antagonists concerning suggestions for their use as future therapeutics.

In recent years, mitochondria have gained significant interest in the field of biomedical research due to their impact on aging, human health, and other advanced findings in metabolic functions. The latest finding shows that metabolic interventions are a leading cause of several diseases, which has sparked interest in finding new therapeutic treatments. Apart from this, the unique inheritance of genetic material from mother to offspring can help scientists find ways to prevent mitochondrial inherited diseases. Additionally, the anti-aging benefits of controlling mitochondrial functions are also being researched. The present study aims to provide a cohesive overview of the latest findings in mitochondrial research, focusing on the role of DRP1 (Dynamin-related protein 1), a member of the GTPase family, in mediating mitochondrial fission. The first section of this paper provides a concise explanation of how DRP1 controls processes such as mitophagy and mitochondrial fission. Subsequently, the paper delves into the topic of inflammation, discussing the current findings regarding the inflammatory response mediated by DRP1. Finally, the role of mitochondrial fission mediated by DRP1 in cancer is examined, reviewing ongoing research on various types of cancer and their recurrence. Moreover, this review also covers the epigenetic regulation of mitochondrial fission. The studies were selected, and evaluated, and the information was collected to present an overview of the key findings. By exploring various aspects of research and potential links, we hope to contribute to a deeper understanding of the intricate relationship between the fields of cancer research and inflammation studies with respect to mitochondrial-based research.