• Differentiating extracellular vesicle (dEV)
• Intermediate mesoderm (IM)
• Kidney differentiation
• Kidney tissue regeneration
• PMEZ scaffold

• 2023R1A2C3003807 Ministry of Science and ICT, South Korea
• 2022R1I1A1A01068486 Ministry of Science and ICT, South Korea
• 23A0206L1 Ministry of Science and ICT, South Korea

• Dehydration
• Infancy
• Kidney transcriptome
• Renal development

• acute kidney injury
• chronic kidney disease
• hyaluronic acid
• injectable hydrogels
• interleukin-10

Mutations in Wilms' tumor 1 (WT1) cause a wide spectrum of renal manifestations, eventually leading to end-stage kidney failure. Insufficient understanding of WT1's molecular functions in kidney development has hampered efficient therapeutic applications for WT1-associated diseases. Recently, the generation and characterization of mouse models and application of multiple state-of-the-art approaches have significantly expanded our understanding of the molecular mechanisms of how WT1 mutations lead to kidney failure. Here, we discuss the WT1 binding consensus and illustrate the major roles of WT1 in different cell populations in kidney biology. WT1 controls metanephric mesenchyme (MM) self-renewal and proliferation mainly by regulating FGF and BMP-pSMAD signaling pathways as well as Sall1 and Pax2, encoding key transcription factors; WT1 drives MM differentiation and mesenchyme–epithelial transition by targeting Fgf8 and Wnt4; WT1 defines podocyte identity by activation of other podocyte-specific transcription factors, including Mafb, Lmx1b, FoxC2, and Tcf21. These factors potentially cooperate with WT1 regulating the expression of components and regulators of the cytoskeleton for establishing podocyte polarity, slit diaphragm structure, and focal adhesion to the glomerular basement membrane. Understanding of WT1's function in kidney biology including WT1-regulated pathways will give insights that will eventually help therapeutic applications.

• Cell type divergence
• Development
• G protein coupled receptors (GPCR)
• Homologs
• Molecular genetics
• Multicellular morphogenesis
• Proportioning
• RasGTP
• Ultrasensitived LEGI

• Cell Shape/genetics
• Chemotaxis/physiology
• Cyclic AMP/metabolism
• Dictyostelium/genetics
• Dictyostelium/physiology
• Extracellular Matrix/metabolism
• Gene Expression Regulation, Developmental/genetics
• Models, Biological
• Morphogenesis/genetics

• P01 GM078586 NIGMS NIH HHS

End stage renal disease (ESRD) is a common disease, which relates to nearly 600 million people in the total population. What is more, it seems to be a crucial problem from the epidemiological point of view. These facts lead to a further necessity of renal replacement therapy development connected with rising expenditures for the health care system. The aim of kidney tissue engineering is to develop and innovate methods of obtaining renal extracellular matrix (ECM) scaffolds derived from kidney decellularization. Recently, progress has been made towards developing a functional kidney graft in vitro on demand. In fact, decellularized tissues constitute ideal natural scaffolds, due to the preservation of native ECM architecture, as well as of cell-ECM binding domains critical in promoting cell attachment, migration, and proliferation. One of the potential sources of the natural scaffolds is the kidney, which cannot be transplanted immediately after excision.

In 2012, about 16487 people received kidney transplants in the United States, whereas 95022 candidates were on the waiting list by the end of the year. Despite advances in renal transplant immunology, approximately 40% of recipients will die or lose graft within 10 years. The limitations of current therapies for renal failure have led researchers to explore the development of modalities that could improve, restore, or replace the renal function. The aim of this paper is to describe a reasonable approach for kidney regeneration and review the current literature regarding cell sources and mechanisms to develop a bioengineering kidney. Due to kidneys peculiar anatomy, extracellular matrix based scaffolds are rational starting point for their regeneration. The perfusion of detergents through the kidney vasculature is an efficient method for delivering decellularizing agents to cells and for removing of cellular material from the tissue. Many efforts have focused on the search of a reliable cell source to provide enrichment for achieving stable renal cell systems. For an efficient bioengineered kidney, these cells must be attached to the organ and then maturated into the bioractors, which simulates the human body environment. A functional bioengineered kidney is still a big challenge for scientists. In the last ten years we have got many improvements on the field of solid organ regeneration; however, we are still far away from the main target. Currently, regenerative centers worldwide have been striving to find feasible strategies to develop bioengineered kidneys. Cell-scaffold technology gives hope to end-stage renal disease patients who struggle with morbidity and mortality due to extended periods on dialysis or immunosupression. The potential of bioengineered organ is to provide a reliable source of organs, which can be refunctionalized and transplanted.

• Kidney regeneration
• Stem cells
• Decellularization
• Extra cellular matrix
• Regenerative medicine