Effect of Caffeine Consumption on Cardiovascular Disease: An Updated Review.

The incidence of cardiovascular diseases has significantly increased with the expansion of the industrialization of societies, which is notably linked to lifestyle changes and an unhealthy diet. Hence, determining the healthiest diet habits and supplements seems to be an appropriate way to decrease the global burden of cardiovascular diseases. Currently, caffeine, one of the most widely consumed compounds in the world, has emerged with some promising results in the treatment of numerous pathophysiological conditions of cardiovascular diseases. A literature search was conducted in PubMed, Scopus, Science Direct, Google Scholar, and Web of Science databases for the relevant articles regarding the pharmacology, preclinical, and clinical studies on the potential effects of caffeine on cardiovascular diseases. While caffeine could improve cardiovascular outcomes through several mechanisms of action, the literature review revealed controversial clinical effects of caffeine on blood pressure, cardiac arrhythmias, acute coronary syndrome, stable angina, and heart failure. In the case of dyslipidemia, coffee consumption increased total cholesterol, triglyceride, and low-density lipoprotein. Taken together, the existence of multiple confounding factors in the caffeine studies has resulted in inconclusive data interpretation. Further well-designed studies with adequate control of the confounding factors are warranted to draw a clear conclusion on the cardiovascular efficacy and safety of caffeine.

Role of Long Non-Coding RNAs in Conferring Resistance in Tumors of the Nervous System.

Tumors of the nervous system can be originated from several locations. They mostly have high mortality and morbidity rate. The emergence of resistance to chemotherapeutic agents is a hurdle in the treatment of patients. Long non-coding RNAs (lncRNAs) have been shown to influence the response of glioblastoma/glioma and neuroblastoma to chemotherapeutic agents. MALAT1, NEAT1, and H19 are among lncRNAs that affect the response of glioma/glioblastoma to chemotherapy. As well as that, NORAD, SNHG7, and SNHG16 have been shown to be involved in conferring this phenotype in neuroblastoma. Prior identification of expression amounts of certain lncRNAs would help in the better design of therapeutic regimens. In the current manuscript, we summarize the impact of lncRNAs on chemoresistance in glioma/glioblastoma and neuroblastoma.

Upregulation of FSHR and PCNA by administration of coenzyme Q10 on cyclophosphamide-induced premature ovarian failure in a mouse model.

Cyclophosphamide (CTX) has been broadly used in the clinic for the treatment of autoimmune disorders and ovarian cancer. The process of chemotherapy has significant toxicity in the reproductive system as it has detrimental effects on folliculogenesis, which leads to an irreversible premature ovarian failure (POF). Coenzyme Q10 (CoQ10) has positive impacts on the reproductive system due to its antioxidant properties, protecting the cells from free-radical oxidative damage and apoptosis. However, little is known about the possible synergistic effect of CTX and CoQ10 on the expression of genes involved in folliculogenesis, such as proliferation cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSHR). A total of 32 NMRI mice were applied and divided into four groups, including healthy control, CTX, CTX + CoQ10, and CoQ10 groups. The effects of CoQ10 on CTX-induced ovarian injury and folliculogenesis were examined by histopathological and real-time quantitative reverse transcription-polymerase chain reaction analyses. The rates of fertilization (in vitro fertilization), embryo development, as well as the level of reactive oxygen species (ROS) in metaphase II (MII) mouse oocytes after PMSG/HCC treatment were also assessed. Results showed that the treatment with CTX decreased the mRNA expression of PCNA and FSHR, IVF rate, and embryo development whereas the application of CoQ10 successfully reversed those factors. CoQ10 administration significantly enhanced histological morphology and decreased ROS levels and the number of atretic follicles in the ovary of CTX-treated mice. In conclusion, it seems that the protective effect of CoQ10 is exerted via the antioxidant and proliferative properties of this substance on CTX-induced ovarian damage.