Globally, kidney disease has become a serious health challenge, with approximately 10% of adults suffering with the disease, and increasing incidence and mortality rates every year. Small extracellular vesicles (sEVs) are 30 nm–100 nm sized nanovesicles released by cells into the extracellular matrix (ECM), which serve as mediators of intercellular communication. Depending on the cell origin, sEVs have different roles which depend on internal cargoes including, nucleic acids, proteins, and lipids. Mesenchymal stem cell (MSCs) exert anti-inflammatory, anti-aging, and wound healing functions mainly via sEVs in a stable and safe manner. MSC-derived sEVs (MSC-sEVs) exert roles in several kidney diseases by transporting renoprotective cargoes to reduce oxidative stress, inhibit renal cell apoptosis, suppress inflammation, and mediate anti-fibrosis mechanisms. Additionally, because MSC-sEVs efficiently target damaged kidneys, they have the potential to become the next generation cell-free therapies for kidney disease. Herein, we review recent research data on how MSC-sEVs could be used to treat kidney disease.

The present study aimed to explore the role of long non-coding (lnc)RNA FTX and ubiquitin-conjugating enzyme E2C (UBE2C) in promoting the progression of renal cell carcinoma (RCC) and the underlying regulatory mechanism. Relative levels of lncRNA FTX, UBE2C, AKT, CDK1 and CDK6 in RCC cell lines were detected by reverse transcription-quantitative (RT-q). Expression levels of UBE2C, phosphorylated (p)-AKT/AKT, p-CDK1/CDK1 and p-CDK6/CDK6 in RCC and paracancerous specimens and RCC cells were measured by western blot or immunohistochemistry assay. In addition, the proliferative rate, cell viability, cell cycle progression, migratory rate and invasive rate of RCC cells overexpressing lncRNA FTX by lentivirus transfection were determined by a series of functional experiments, including the colony formation assay, MTT assay, flow cytometry, Transwell assay and wound healing assay. The targeted binding relationship in the lncRNA FTX/miR-4429/UBE2C axis was validated by dual-luciferase reporter assay. By intervening microRNA (miR)-4492 and UBE2C by the transfection of miR-4429-mimics or short interfering UBE2C-2, the regulatory effect of lncRNA FTX/miR-4429/UBE2C axis on the progression of RCC was evaluated. Finally, a xenograft model of RCC in nude mice was established by subcutaneous implantation, thus evaluating the in vivo function of lncRNA FTX in the progression of RCC. The results showed that lncRNA FTX and UBE2C were upregulated in RCC specimens and cell lines. The overexpression of lncRNA FTX in RCC cells upregulated UBE2C. In addition, the overexpression of lncRNA FTX promoted the cell viability and proliferative, migratory and invasive capacities of RCC cells and accelerated the cell cycle progression. A dual-luciferase reporter assay validated that lncRNA FTX exerted the miRNA sponge effect on miR-4429, which was bound to UBE2C 3'UTR. Knockdown of UBE2C effectively reversed the regulatory effects of overexpressed lncRNA FTX on the abovementioned phenotypes of RCC cells. In the xenograft model of RCC, the mice implanted with RCC cells overexpressing lncRNA FTX showed a larger tumor size and higher tumor weight than those of controls, while the in vivo knockdown of UBE2C significantly reduced the size of RCC lesions, indicating the reversed cancer-promoting effect of lncRNA FTX. Overall, the present study showed that lncRNA FTX was upregulated in RCC and could significantly promote the proliferative, migratory and invasive capacities, enhancing the viability and accelerating the cell cycle progression of RCC cells by exerting the miRNA sponge effect on miR-4429 and thus upregulating UBE2C. lncRNA FTX and UBE2C are potential molecular biomarkers and therapeutic targets of RCC.

Type 2 diabetes is one of the most common chronic diseases in modern society. However, there is still insufficient research on the pathogenesis, diagnosis and treatment of type 2 diabetes and its complications. Extracellular vesicles are small bilayer vesicles secreted by cells. In recent years, the effect of extracellular vesicles in type 2 diabetes and its complications has aroused extensive attention. The research on the influence of protein and nucleic acids carried by extracellular vesicles secreted by stem cells and inflammatory cells on the pathogenesis of type 2 diabetes and its complications provides new ideas for its diagnosis and treatment. This review focuses on the influence of extracellular vesicles on insulin resistance by regulating inflammation and glucose transporter 4 expression. The second part mainly discusses the research progress and limitations of extracellular vesicles use in treating and diagnosing type 2 diabetes and its complications. This review introduces the current research status of type 2 diabetes and its complications, illustrates the biogenesis of extracellular vesicles, their effect on type 2 diabetes pathogenesis and its complications and their potential as therapeutic tools and diagnostic markers in type 2 diabetes and its complications.

Renal cell carcinoma (RCC) represents an extremely challenging disease in terms of both diagnosis and treatment. It poses a significant threat to human health, with incidence rates increasing at a yearly rate of roughly 2%. Extracellular vesicles (EVs) are lipid-based bilayer structures of membranes that are essential for intercellular interaction and have been linked to the advancement of RCC. This review provides an overview of recent studies on the role of EVs in RCC progression, including involvement in the interaction of tumor cells with M2 macrophages, mediating the generation of immune tolerance, and assuming the role of communication messengers in the tumor microenvironment leading to disease progression. Finally, the “ troika “ of EVs in RCC therapy is presented, including engineered sEVs’ or EVs tumor vaccines, mesenchymal stem cell EVs therapy, and reduction of tumor-derived EVs secretion. In this context, we highlight the limitations and challenges of EV-based research and the prospects for future developments in this field. Overall, this review provides a comprehensive summary of the role of EVs in RCC and their potential as a viable pathway for the future treatment of this complex disease.