Metabolic programming of nephron progenitor cell fate
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REVIEW
Metabolic programming of nephron progenitor cell fate Giovane G Tortelote 1 & Mariel Colón-Leyva 1 & Zubaida Saifudeen 1 Received: 1 May 2020 / Revised: 30 June 2020 / Accepted: 31 August 2020 # IPNA 2020
Abstract Metabolic pathways are one of the first responses at the cellular level to maternal/fetal interface stressors. Studies have revealed the previously unrecognized contributions of intermediary metabolism to developmental programs. Here, we provide an overview of cellular metabolic pathways and the cues that modulate metabolic states. We discuss the developmental and physiological implications of metabolic reprogramming and the key role of metabolites in epigenetic and epiproteomic modifications during embryonic development and with respect to kidney development and nephrogenesis. Keywords Metabolic plasticity . Embryonic kidney . Development . Glycolysis . OxPhos . Metabolites . Epiproteome . Epigenome
Abbreviations α-KG Alpha ketoglutarate CAKUT Congenital abnormalities of kidney and urinary tract CM Cap mesenchyme CKD Chronic kidney disease CVD Cardiovascular disease ESC Embryonic stem cell FAD Flavin adenine dinucleotide GFR Glomerular filtration rate HBP Hexosamine biosynthesis pathway HSPG Heparan sulfate proteoglycans JmjC Jumonji C-domain containing protein family of demethylases LSD Lysine-specific demethylase MM Metanephric mesenchyme MPC1/2 Mitochondrial pyruvate carrier NAD Nicotinamide adenine dinucleotide NPC Nephron progenitor cells PFKFB3 6- Pho spho fructo -2-k inase /f ructo se-2, 6bisphosphatase PPP Pentose phosphate pathway PSC Pluripotent stem cells * Zubaida Saifudeen [email protected] 1
Department of Pediatrics, Tulane University School of Medicine, 1430 Tulane Avenue SL37, Room 5534, New Orleans, LA 70112, USA
PTM RTK SAM TCA UB VHL
Posttranslational modification Receptor tyrosine kinase S-Adenosyl methionine Tricarboxylic acid cycle Ureteric bud Von Hippel–Lindau tumor suppressor
Introduction The kidney is the primary organ responsible for the excretion of toxic cellular waste as well as the regulator of the body’s water levels, osmolarity, blood pressure, and mineral balance. The nephron is the functional unit of the kidney, and accordingly, kidney function is proportional to nephron number. Although the absolute nephron number required to maintain healthy kidney function is not known, low nephron number is a documented risk factor for diminishing glomerular filtration rate (GFR), development of chronic kidney disease (CKD), and an increased propensity to cardiovascular disease (CVD). Associative evidence links the maternal environment during gestation to fetal growth and organogenesis. Fluctuations in the maternal environment, such as gestational diabetes or preeclampsia, negatively impact fetal nephron endowment [1–3]. Maternal nutritional deprivation during gestation is also a documented modifier of fetal growth [4]. Impaired renewal or differentiation of nephron progenitor cells (NPC) can impede nephrogenesis and result in nephron deficit and hypoplasia of the ki
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