2022
DOI: 10.3390/antiox11020356
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Abstract: Chronic kidney disease (CKD) is a world health problem increasing dramatically. The onset of CKD is driven by several mechanisms; among them, metabolic reprogramming and changes in redox signaling play critical roles in the advancement of inflammation and the subsequent fibrosis, common pathologies observed in all forms of CKD. Extracellular vesicles (EVs) are cell-derived membrane packages strongly associated with cell-cell communication since they transfer several biomolecules that serve as mediators in redo… Show more

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Cited by 10 publications
(8 citation statements)
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References 189 publications
(451 reference statements)
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“…Some uremic toxins (i.e., indole acetic acid, Indoxyl sulfate, p -cresyl sulfate) can increase ROS production, enhancing oxidative stress in CKD patients. This leads to proteins, lipids, and DNA modifications, many of which are composed of protein carbonyl compounds, which are precursors of pentosidine, which derives from protein and lipids oxidation and glycation [ 43 , 44 , 45 ]. Uremic patients, in fact, show a deficiency of glyoxalase I (GLO-I), failing to detoxify reactive carbonyl compounds, determining increased levels of AGEs in these patients [ 9 ].…”
Section: Discussionmentioning
confidence: 99%
“…Some uremic toxins (i.e., indole acetic acid, Indoxyl sulfate, p -cresyl sulfate) can increase ROS production, enhancing oxidative stress in CKD patients. This leads to proteins, lipids, and DNA modifications, many of which are composed of protein carbonyl compounds, which are precursors of pentosidine, which derives from protein and lipids oxidation and glycation [ 43 , 44 , 45 ]. Uremic patients, in fact, show a deficiency of glyoxalase I (GLO-I), failing to detoxify reactive carbonyl compounds, determining increased levels of AGEs in these patients [ 9 ].…”
Section: Discussionmentioning
confidence: 99%
“…Hemodynamic alterations appear immediately after surgery [ 46 , 47 ], as well as renal perfusion changes and increased oxygen consumption, inducing metabolic shift [ 48 , 49 , 50 ] and increased ATP demand [ 34 , 49 ]. The lipotoxicity and mitochondrial impairment in the kidneys [ 51 , 52 , 53 ] triggering metabolic reprogramming is characterized by the shift from mitochondrial-based to anaerobic metabolism, a key mechanism commonly observed in CKD progression [ 54 , 55 , 56 ]. Nephron sites with a high dependence on mitochondria are among the most affected by the accumulation of lipid deposits [ 53 , 57 ].…”
Section: Discussionmentioning
confidence: 99%
“…Until now, the pathological mechanisms that trigger CKD and its progression had not been completely elucidated [ 5 ]. Previous literature has revealed some potential factors that may be involved in CKD progression, such as oxidative stress, ectopic lipid accumulation, dyslipidemia, renal cell damage and dysfunction, and others [ 6 , 7 , 8 , 9 ].…”
Section: Introductionmentioning
confidence: 99%