There is no doubt that the incidence of cancer sufferers is rising in the world, and it is estimated that in the next several decades, the number of people suffering from malignancies or the cancer rate will double. Diagnostic and therapeutic targeting of noncoding RNAs (ncRNAs), especially microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), represent an excellent approach for cancer diagnosis and treatment, as well as many other diseases. One of the latest miRNAs is miR-4492, upregulating some genes in tumor tissues including ROMO1, HLA-G, NKIRAS2, FOXK1, and UBE2C.It represents an attractant example of a miRNA acting at multiple levels to affect the same malignancy hallmark. Based on the studies, miR-4492 plays a key role in several cancers such as, breast cancer, bladder cancer, osteosarcoma, glioblastoma multiforme, hepatocellular carcinoma, colorectal cancer, and ovarian cancer. Putting it all together, identifying the precise mechanisms of miR-4492 in the pathogenesis of cancer, could pave the way to find better diagnostic and therapeutic strategies for cancer sufferers. For this reason, it might be a novel potential diagnostic biomarker and therapeutic target for neoplasms.

One of the most complicated eye disorders is age-related macular degeneration (AMD) which is the leading cause of irremediable blindness all over the world in the elderly.AMD is classified as early stage to late stage (advanced AMD), in which this stage is divided into the exudative or neovascular form (wet AMD) and the nonexudative or atrophic form (dry AMD). Clinically, AMD primarily influences the central area of retina known as the macula. Importantly, the wet form is generally associated with more severe vision loss. AMD has a systemic component, where many factors, like aging, genetic, environment, autoimmune and non-autoimmune disorders are associated with this disease. Additionally, healthy lifestyles, regular exercise, maintaining a normal lipid profile and weight are crucial to decreasing the risk of AMD. Furthermore, therapeutic strategies for limiting AMD should encompass a variety of factors to avoid and improve drug interventions, and also need to take into account personalized genetic information. In conclusion, with the development of technology and research progress, visual impairment and legal blindness from AMD have been substantially reduced in incidence. This review article is focused on identifying and developing the knowledge about the association between genetics, and etiology with AMD. We hope that this review will encourage researchers and lecturers, open new discussions, and contribute to a better understanding of AMD that improves patients’ visual acuity, and upgrades the quality of life of AMD patients.

Contrast-induced acute kidney injury (CI-AKI) is a frequent challenge following the injection of contrast media and its subsequent oxidative stress. The aim of the present study was to evaluate the preventive effects of coenzyme Q10 (Q10), as a mitochondrial-targeted antioxidant in CI-AKI in diabetic patients, who account for a large proportion of angiographic cases. A total of 118 diabetic patients were randomly assigned to receive 120 mg of oral coenzyme Q10 (Q10 group) or placebo (Placebo group) for four days, starting 24 hours before contrast media injection. Blood urea nitrogen (BUN), serum and urinary creatinine, estimated glomerular filtration rate (eGFR), urinary malondialdehyde (UMDA), urinary total antioxidant capacity (UTAC), and urinary mitochondrial to nuclearDNA ratios (mtDNADNA ratio) were evaluated before and after the treatment period. Urine sediments were also evaluated to report the urine microscopy score (UMS).The levels of BUN, serum and urine creatinine, and UMS were similar in the Q10 and placebo groups. EGFR was lower in the Q10 group before the treatment (p=0.013) but not after. The urinary mtDNADNA ratio was 3.05±1.68 and 3.69±2.58 in placebo and Q10 groups, but UTAC was found to be lower in Q10 both before (p=0.006) and after the treatment (p＜0.001). The incidence of CI-AKI was 14.40% and the mtDNANDA ratio was similar between CI-AKI and non-CI-AKI patients. In conclusion, Q10 treatment shows no favorable effect on prevention of CI-AKI or a urinary mtDNADNA ratio among diabetic patients.