TY - JOUR
T1 - Sarcopenia in chronic kidney disease
T2 - Focus on advanced glycation end products as mediators and markers of oxidative stress
AU - Dozio, Elena
AU - Vettoretti, Simone
AU - Lungarella, Giuseppe
AU - Messa, Piergiorgio
AU - Romanelli, Massimiliano M.Corsi
N1 - Funding Information:
Funding: The study was supported by Ricerca Corrente funding from Italian Ministry of Health to IRCCS Policlinico San Donato.
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/4
Y1 - 2021/4
N2 - Sarcopenia is common in chronic kidney disease (CKD), and it is independently associated with morbidity and mortality. Advanced glycation end products (AGE) are mainly known as aging products. In CKD, AGE accumulate due to increased production and reduced kidney excretion. The imbalance between oxidant/antioxidant capacities in CKD patients is one of the main factors leading to AGE synthesis. AGE can, in turn, promote CKD progression and CKD-related complications by increasing reactive oxygen species generation, inducing inflammation, and promoting fibrosis. All these derangements can further increase AGE and uremic toxin accumulation and promote loss of muscle mass and function. Since the link between AGE and sarcopenia in CKD is far from being fully understood, we revised hereby the data supporting the potential contribution of AGE as mediators of oxidative stress in the pathogenesis of sarcopenia. Understanding how AGE and oxidative stress impact the onset of sarcopenia in CKD may help to identify new potential markers of disease progression and/or therapeutic targets.
AB - Sarcopenia is common in chronic kidney disease (CKD), and it is independently associated with morbidity and mortality. Advanced glycation end products (AGE) are mainly known as aging products. In CKD, AGE accumulate due to increased production and reduced kidney excretion. The imbalance between oxidant/antioxidant capacities in CKD patients is one of the main factors leading to AGE synthesis. AGE can, in turn, promote CKD progression and CKD-related complications by increasing reactive oxygen species generation, inducing inflammation, and promoting fibrosis. All these derangements can further increase AGE and uremic toxin accumulation and promote loss of muscle mass and function. Since the link between AGE and sarcopenia in CKD is far from being fully understood, we revised hereby the data supporting the potential contribution of AGE as mediators of oxidative stress in the pathogenesis of sarcopenia. Understanding how AGE and oxidative stress impact the onset of sarcopenia in CKD may help to identify new potential markers of disease progression and/or therapeutic targets.
KW - Advanced glycation end products (AGE)
KW - Chronic kidney disease
KW - Oxidative stress
KW - Sarcopenia
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U2 - 10.3390/biomedicines9040405
DO - 10.3390/biomedicines9040405
M3 - Article
AN - SCOPUS:85104838779
VL - 9
JO - Biomedicines
JF - Biomedicines
SN - 2227-9059
IS - 4
M1 - 405
ER -