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The prevalence of chronic kidney disease (CKD) increased by 88% from 1990 to 2016. Age of onset of lifestyle-related diseases (such as hypertension, diabetes mellitus, obesity, dyslipidemia, and hyperuricemia), which are risk factors for incident CKD, is lower now compared with the past. Thus, we aimed to evaluate the risk factors for the incidence and progression of CKD in the young and middle-aged population. There are differences in the risk for CKD among the young, middle-aged, and elderly populations. We aimed to assess obesity (which is basic component of metabolic syndrome), waist circumference, and abdominal adiposity, which are predictive factors of CKD in the younger population. Furthermore, we described the management and clinical evidence of hypertension, diabetes mellitus, dyslipidemia, and hyperuricemia for young and middle-aged patients, along with diet management and nutrients associated with kidney function. Kidney function in the young and middle-aged population is mostly normal, and they are considered a low-risk group for incident CKD. Thus, we expect this review to be useful in reducing the prevalence of CKD.

Mitochondria are important cellular organelles that function as control centers of the energy supply for highly proliferative cancer cells and regulate apoptosis after cancer chemotherapy. Cisplatin is one of the most important chemotherapeutic agents and a key drug in therapeutic regimens for a broad range of solid tumors. Cisplatin may directly interact with mitochondria, which can induce apoptosis. The direct interactions between cisplatin and mitochondria may account for our understanding of the clinical activity of cisplatin and development of resistance. However, the basis for the roles of mitochondria under treatment with chemotherapy is poorly understood. In this review, we present novel aspects regarding the unique characteristics of the mitochondrial genome in relation to the use of platinum-based chemotherapy and describe our recent work demonstrating the importance of the mitochondrial transcription factor A (mtTFA) expression in cancer cells.

We previously reported that the transcription factor Zinc Finger Protein 143 (ZNF143) regulates the expression of genes associated with cell cycle and cell division, and that downregulation of ZNF143 induces cell cycle arrest at G2/M. To assess the function of ZNF143 expression in the cell cycle, we established two cells with forced expression of ZNF143 derived from PC3 prostate cancer cell lines. These cell lines overexpress genes associated with cell cycle and cell division, such as polo-like kinase 1 (PLK1), aurora kinase B (AURKB) and some minichromosome maintenance complex components (MCM). However, the doubling time of cells with forced expression of ZNF143 was approximately twice as long as its control counterpart cell line. Analysis following serum starvation and re-seeding showed that PC3 cells were synchronized at G1 in the cell cycle. Also, ZNF143 expression fluctuated, and was at its lowest level in G2/M. However, PC3 cells with forced expression of ZNF143 synchronized at G2/M, and showed lack of cell cycle-dependent fluctuation of nuclear expression of MCM proteins. Furthermore, G2/M population of both cisplatin-resistant PCDP6 cells over-expressing ZNF143 (derived from PC3 cells) and cells with forced expression of ZNF143 was significantly higher than that of each counterpart, and the doubling time of PCDP6 cells is about 2.5 times longer than that of PC3 cells. These data suggested that fluctuations in ZNF143 expression are required both for gene expression associated with cell cycle and for cell division.