Advanced glycation end products are associated with sarcopenia in older women: aging marker dynamics

Eguchi, Yawara; Toyoguchi, Toru; Inage, Kazuhide; Fujimoto, Kazuki; Orita, Sumihisa; Suzuki, Miyako; Kanamoto, Hirohito; Abe, Koki; Norimoto, Masaki; Umimura, Tomotaka; Koda, Masao; Furuya, Takeo; Aoki, Yasuchika; Nakamura, Junichi; Akazawa, Tsutomu; Takahashi, Kazuhisa; Ohtori, Seiji

doi:10.1080/08952841.2019.1697161

Cited by 30 publications

(51 citation statements)

References 34 publications

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“…Interestingly, this type of modification was also observed in old human M. vastus lateralis (~78 years old) when compared with young (~25 years old) [ 35 ]. Remarkably, this was also the case in serum of elderly patients and it was found to be correlated with loss of lean mass [ 33 ]. Another posttranslational protein modification that we detected was K63-polyubiquitination, a key event that directs proteins to autophagy.…”

Section: Discussionmentioning

confidence: 80%

“…Nevertheless, there was also a higher amount of 3-NT in old EDL, yet it did not reach statistical significance. Among other posttranslational oxidative modifications, we investigated a product of glycosylation, pentosidine, known as advanced glycation end product and known to favor protein aggregation [ 33 , 34 ]. Pentosidine was found to be significantly increased in both muscle fiber types in old mice ( Figure 1(b) ).…”

Section: Discussionmentioning

confidence: 99%

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Age-Related Maintenance of the Autophagy-Lysosomal System Is Dependent on Skeletal Muscle Type

Fernando

Castro

Flore

et al. 2020

Oxidative Medicine and Cellular Longevity

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The skeletal muscle plays an important role in maintaining whole-body mechanics, metabolic homeostasis, and interorgan crosstalk. However, during aging, functional and structural changes such as fiber integrity loss and atrophy can occur across different species. A commonly observed hallmark of aged skeletal muscle is the accumulation of oxidatively modified proteins and protein aggregates which point to an imbalance in proteostasis systems such as degradation machineries. Recently, we showed that the ubiquitin-proteasomal system was impaired. Specifically, the proteasomal activity, which was declining in aged M. soleus (SOL) and M. extensor digitorum longus (EDL). Therefore, in order to understand whether another proteolytic system would compensate the decline in proteasomal activity, we aimed to investigate age-related changes in the autophagy-lysosomal system (ALS) in SOL, mostly consisting of slow-twitch fibers, and EDL, mainly composed of fast-twitch fibers, from young (4 months) and old (25 months) C57BL/6JRj mice. Here, we focused on changes in the content of modified proteins and the ALS. Our results show that aged SOL and EDL display high levels of protein modifications, particularly in old SOL. While autophagy machinery appears to be functional, lysosomal activity declines gradually in aged SOL. In contrast, in old EDL, the ALS seems to be affected, demonstrated by an increased level of key autophagy-related proteins, which are known to accumulate when their delivery or degradation is impaired. In fact, lysosomal activity was significantly decreased in old EDL. Results presented herein suggest that the ALS can compensate the high levels of modified proteins in the more oxidative muscle, SOL, while EDL seems to be more prone to ALS age-related alterations.

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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Age-Related Maintenance of the Autophagy-Lysosomal System Is Dependent on Skeletal Muscle Type

Fernando

Castro

Flore

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Although various instruments to measure SAF have been developed, the use of SAF to assess AGE levels is controversial. Some reports found no correlation between SAF and serum AGEs [26][27][28]. On the other hand, several reports showed that both serum pentosidine and SAF were signi cantly increased in patients with T2DM [16] and those undergoing hemodialysis [15].…”

Section: Discussionmentioning

confidence: 99%

Associations Between Skin Autofluorescence, Advanced Glycation End-Products and Chronic Low Back Pain

Umimura

Eguchi

Inage

et al. 2020

Preprint

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Objective: The aim of this study was to determine whether advanced glycation end-products (AGEs) measured by skin autofluorescence (SAF) can serve as a biomarker for chronic low back pain. 111 patients who visited the outpatient clinic were included in this prospective cohort study. They were divided into a chronic low back pain group (C group: 48 patients, mean age 52.2) and a group without low back pain (N group: 63 healthy volunteers, mean age 40.8). SAF was measured as a parameter of AGEs using an autofluorescence reader. Measurements of low back pain visual analog scale (VAS), presence of diabetes, and SAF were recorded, and correlations between VAS or diabetes and SAF were investigated. Results: The C group had significantly higher SAF (2.20 vs 1.97, p<0.05) than the N group, whereas the SAF for diabetes patients was significantly higher (2.7 vs 2.1, p<0.05) than subjects without diabetes. SAF had no correlation with VAS (P=0.18). SAF is an indicator of AGE accumulation correlated with chronic low back pain and diabetes.

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“…Previous studies conducted in settings different from CKD [ 10 , 11 , 12 , 13 ] demonstrated that the accumulation of advanced glycation end products (AGE) was strongly related to oxidative stress and could impact muscle function. Thus, it is plausible that AGE may contribute to the onset and progression of sarcopenia in CKD as well [ 14 ].…”

Section: Sarcopenia In Chronic Kidney Disease: Potential Mechanismsmentioning

confidence: 99%

“…Presently, most of the knowledge on how AGE affect muscle function and about what could be their role in the onset and progression of sarcopenia comes from in vitro works, animal studies, and clinical observations in DM, cancer, and aging [ 10 , 11 , 12 ]. Healthy muscle contains myoblasts that differentiate into myotubes.…”

Section: Age In Ckd: Pathogenetic Rolementioning

confidence: 99%

Sarcopenia in Chronic Kidney Disease: Focus on Advanced Glycation End Products as Mediators and Markers of Oxidative Stress

et al. 2021

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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.

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Advanced glycation end products are associated with sarcopenia in older women: aging marker dynamics

Cited by 30 publications

References 34 publications

Age-Related Maintenance of the Autophagy-Lysosomal System Is Dependent on Skeletal Muscle Type

Age-Related Maintenance of the Autophagy-Lysosomal System Is Dependent on Skeletal Muscle Type

Associations Between Skin Autofluorescence, Advanced Glycation End-Products and Chronic Low Back Pain

Sarcopenia in Chronic Kidney Disease: Focus on Advanced Glycation End Products as Mediators and Markers of Oxidative Stress

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