Cell Metabolism, Journal Year: 2023, Volume and Issue: 35(12), P. 2165 - 2182.e7
Published: Dec. 1, 2023
Language: Английский
Cell Metabolism, Journal Year: 2020, Volume and Issue: 32(3), P. 404 - 419.e6
Published: July 28, 2020
Language: Английский
Citations
269
Nature Reviews Nephrology, Journal Year: 2020, Volume and Issue: 17(3), P. 153 - 171
Published: Sept. 22, 2020
Language: Английский
Citations
186
Kidney International, Journal Year: 2025, Volume and Issue: 107(2), P. S1 - S239
Published: Jan. 21, 2025
Language: Английский
Citations
6
Clinical Journal of the American Society of Nephrology, Journal Year: 2020, Volume and Issue: 15(4), P. 577 - 584
Published: Feb. 21, 2020
Autosomal dominant polycystic kidney disease is characterized by progressive development and enlargement of cysts, leading to ESKD. Because the kidneys are under high metabolic demand, it not surprising that mounting evidence suggests a defect exists in vitro animal models autosomal disease, which likely contributes cystic epithelial proliferation subsequent cyst growth. Alterations include defective glucose metabolism (reprogramming favor aerobic glycolysis), dysregulated lipid amino acid metabolism, impaired autophagy, mitochondrial dysfunction. Limited supports cellular also humans with disease. There notable overlapping features pathways among obesity, and/or Both dietary pharmacologic-based strategies targeting abnormalities being considered as therapies slow progression attractive, particularly given slowly nature Dietary daily caloric restriction, intermittent fasting, time-restricted feeding, ketogenic diet, 2-deoxy-glucose well alterations nutrient availability. Pharmacologic-based AMP-activated kinase activators, sodium cotransporter-2 inhibitors, niacinamide, thiazolidenediones. The results from initial clinical trials upcoming anxiously awaited within scientific communities. continues be need for additional mechanistic studies better understand role translation trials. Beyond single-intervention focused on reprograming great potential combining metabolic-focused therapeutic approaches compounds other signaling cascades altered such tolvaptan.
Language: Английский
Citations
92
Kidney International, Journal Year: 2021, Volume and Issue: 100(5), P. 1037 - 1053
Published: July 8, 2021
Language: Английский
Citations
91
Nature Genetics, Journal Year: 2021, Volume and Issue: 53(12), P. 1649 - 1663
Published: Oct. 11, 2021
Language: Английский
Citations
88
Cellular Signalling, Journal Year: 2019, Volume and Issue: 67, P. 109495 - 109495
Published: Dec. 6, 2019
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a slowly progressive disease characterized by the relentless growth of renal cysts throughout life affected individuals. Early evidence suggested that epithelia lining share neoplastic features, leading to definition PKD as "neoplasm in disguise". Recent work from our and other laboratories has identified profound metabolic reprogramming PKD, similar one reported cancer consistent with increased proliferation. Multiple lines suggest aerobic glycolysis (a Warburg-like effect) present disease, along dysfunctions such an increase pentose phosphate pathway, glutamine anaplerosis fatty acid biosynthesis, while oxidation oxidative phosphorylation (OXPHOS) are decreased. In addition glutamine, amino acid-related pathways appear altered, including asparagine arginine. The precise origin alterations not entirely clear, but two hypotheses can be formulated, mutually exclusive. First, polycystins have been recently shown regulate directly mitochondrial function structure either regulating Ca2+ uptake mitochondria at Mitochondria Associated Membranes (MAMs) Endoplasmic Reticulum, or direct translocation small fragment protein into matrix mitochondria. One alternative possibility ADPKD secondary de-regulation proliferation, driven multiple signaling which include mTORC1 AMPK among most relevant. While mechanisms underlying these novel will need further investigation, it evident they offer great opportunity for interventions disease.
Language: Английский
Citations
87
Kidney International, Journal Year: 2019, Volume and Issue: 95(5), P. 1253 - 1261
Published: March 4, 2019
Language: Английский
Citations
80
Advanced Science, Journal Year: 2021, Volume and Issue: 8(9)
Published: March 1, 2021
Atherosclerosis is a chronic inflammatory disease that can cause acute cardiovascular events. Activation of the NOD-like receptor family, pyrin domain containing protein 3 (NLRP3) inflammasome enhances atherogenesis, which links lipid metabolism to sterile inflammation. This study examines impact an endogenous metabolite, namely ketone body 3-hydroxybutyrate (3-HB), on mouse model atherosclerosis. It found daily oral administration 3-HB significantly ameliorate Mechanistically, reduce M1 macrophage proportion and promote cholesterol efflux by acting macrophages through its G-protein-coupled 109a (Gpr109a). 3-HB-Gpr109a signaling promotes extracellular calcium (Ca2+) influx. The elevation intracellular Ca2+ level reduces release from endothelium reticulum (ER) mitochondria, thus inhibits ER stress triggered store depletion. As NLRP3 be activated stress, inhibit activation inflammasome, triggers increase inhibition efflux. concluded nutritional supplementation attenuates atherosclerosis in mice.
Language: Английский
Citations
70
Cell Metabolism, Journal Year: 2021, Volume and Issue: 33(6), P. 1234 - 1247.e7
Published: April 15, 2021
Language: Английский
Citations
69