Nuclear reprogramming has reshaped stem cell science and created new avenues for cell-based therapies. The ability to bestow any given phenotype upon adult cells regardless of their origin is an exciting possibility. How can this powerful tool be harnessed for the treatment of kidney disease? Many approaches, including induced pluripotent stem cell (iPSC) production, direct lineage conversion, and reprogramming to a kidney progenitor, are now possible. Indeed, the generation of iPSC lines from adult kidney-derived cells has been successfully achieved. This, however, is just the beginning of the challenge. This review will discuss the fundamental concepts of transcription factor-based reprogramming in its various forms, highlighting recent advances in the field and how these are applicable to the kidney. The relative merits of each approach will be discussed in the context of what is a realistic and feasible strategy for kidney regeneration via reprogramming.
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http://dx.doi.org/10.1038/ki.2012.68 | DOI Listing |
Stem Cell Res
December 2024
Kidney and Urinary Tract Center, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH, USA. Electronic address:
Cloaca is an ultra-rare severe anorectal malformation in females where the gastrointestinal, genital, and urologic systems converge. Posterior Cloaca (Type B) is an extremely rare specific variant, where the urogenital sinus opens just anterior to the anus. NCHi027-A is an iPSC line derived from skin fibroblasts of a 4 year and 8-month-old female with Posterior Cloaca (Type B) using Sendai Virus reprogramming.
View Article and Find Full Text PDFCell Rep Med
December 2024
Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands; Oncode Institute, Utrecht, the Netherlands. Electronic address:
Malignant rhabdoid tumor (MRT) is one of the most aggressive childhood cancers for which no effective treatment options are available. Reprogramming of cellular metabolism is an important hallmark of cancer, with various metabolism-based drugs being approved as a cancer treatment. In this study, we use patient-derived tumor organoids (tumoroids) to map the metabolic landscape of several pediatric cancers.
View Article and Find Full Text PDFBiol Direct
December 2024
Department of Urology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, 3 Qingchun Road, Hangzhou, 310016, China.
Background: Precision oncology's implementation in clinical practice faces significant constraints due to the inadequacies in tools for detailed patient stratification and personalized treatment methodologies. Dysregulated tryptophan metabolism has emerged as a crucial factor in tumor progression, encompassing immune suppression, proliferation, metastasis, and metabolic reprogramming. However, its precise role in clear cell renal cell carcinoma (ccRCC) remains unclear, and predictive models or signatures based on tryptophan metabolism are conspicuously lacking.
View Article and Find Full Text PDFChem Biol Interact
December 2024
Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Department of Clinical Pharmacology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, 310006, China. Electronic address:
As the development of nanotechnology, the application of nanoproducts and the advancement of nanomedicine, the contact of nanoparticles (NPs) with human body is becoming increasingly prevalent. This escalation elevates the risk of NPs exposure for workers, consumers, researchers, and both aquatic and terrestrial organisms throughout the production, usage, and disposal stages. Consequently, evaluating nanotoxicity remains critically important, though standardized assessment criteria are still lacking.
View Article and Find Full Text PDFKidney Int Rep
December 2024
INSERM Centre d'Investigation Clinique 1402, CHU Poitiers, University of Poitiers, Poitiers, France.
Mitochondria are essential for cellular energy production and are implicated in numerous diseases, including diabetic kidney disease (DKD). Current evidence indicates that mitochondrial dysfunction results in alterations in several metabolic pathways within kidney cells, thereby contributing to the progression of DKD. Furthermore, mitochondrial dysfunction can engender an inflammatory milieu, leading to the activation and recruitment of immune cells to the kidney tissue, potentially perturbing intrarenal metabolism.
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