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Myosteatosis and not low muscle mass is associated with lower survival in kidney transplant recipients 在肾移植受者中，肌骨增生和非低肌肉质量与较低的生存率相关
JCSM rapid communications
Pub Date : 2024-05-31 DOI: 10.1002/rco2.96
Kristoffer N.D. Huitfeldt Sola, Helena M. Genberg, Carla M. Avesani, Torkel B. Brismar

Background

Myosteatosis, that is muscle fat infiltration, is an important marker of muscle quality, affecting quality of life and survival in patients with chronic kidney disease (CKD). However, the connection between myosteatosis, skeletal muscle index (SMI) and survival in kidney transplant (KTx) recipients remains unclear.

Methods

This retrospective observational study included a cohort of consecutive adult kidney recipients transplanted between 2010 and 2017 in Stockholm. Preoperative abdominal computed tomography (CT) images obtained after diagnosis of CKD 5 and within 36 months of transplantation were collected. Using established criteria, we measured muscle area at the third lumbar vertebra (L3 level) and identified low attenuation muscle, indicating myosteatosis. Each area was divided by height squared providing the SMI, and fatty muscle index (FMI). Given that there is no commonly accepted definition of sarcopenia, two cut-offs for SMI were used to define low muscle mass, Cut-off 1 (≤32.8 for women and ≤44.7 for men) and Cut-off 2 (≤38.5 for women and ≤52.4 for men). Average radiodensity of skeletal muscle and Charlson comorbidity index were calculated for each patient. The influence on survival from SMI, FMI, SMI/FMI ratio, and radiodensity was analysed.

Results

Out of 582 KTx recipients, 266 (46%) had a pre-transplant abdominal CT available. Applying SMI Cut-off 1, 30 recipients (11%) had sarcopenia compared with 106 (40%) with Cut-off 2. Neither SMI nor FMI was associated with survival. Yet there was an association between SMI/FMI ratio and survival, patients with the lowest quintile SMI/FMI ratio having a significantly lower survival when compared with the highest quintile, both in the crude model and when adjusted for age, gender, and comorbidity. Additionally, FMI, radiodensity, and SMI/FMI, but not SMI, were significantly associated with Charlson comorbidity index (P < 0.01).

Conclusions

The SMI/FMI ratio may be associated with both pre-transplant comorbidity and post-transplant survival even though the significance of SMI is unclear. This suggests that SMI/FMI ratio is a better indicator of muscular impairment than skeletal muscle quantity alone. The finding may reflect the complex interplay between muscle mass, muscular fat infiltration and metabolic health, all important determinants of wellness and longevity. In summary, our study underscores the potential of the SMI/FMI ratio a

背景肌肥大症，即肌肉脂肪浸润，是肌肉质量的重要标志，影响慢性肾脏疾病（CKD）患者的生活质量和生存。然而，肾移植（KTx）受者骨骼肌指数（SMI）和存活之间的关系尚不清楚。方法：本回顾性观察性研究纳入了2010年至2017年在斯德哥尔摩连续移植的成人肾受体队列。收集CKD 5诊断后及移植36个月内术前腹部CT图像。使用既定标准，我们测量了第三腰椎（L3水平）的肌肉面积，并确定了低衰减肌肉，表明肌骨化症。每个区域除以身高的平方，给出SMI和脂肪肌肉指数（FMI）。鉴于肌少症没有一个普遍接受的定义，我们使用了SMI的两个临界值来定义低肌肉量，临界值1（女性≤32.8，男性≤44.7）和临界值2（女性≤38.5，男性≤52.4）。计算每位患者骨骼肌平均放射密度和Charlson合并症指数。分析SMI、FMI、SMI/FMI比值和放射密度对生存率的影响。结果在582例KTx受者中，266例（46%）有移植前腹部CT。应用SMI cut - t1, 30名接受者（11%）出现肌肉减少症，而cut - t2有106名接受者（40%）出现肌肉减少症。SMI和FMI都与生存无关。然而，在SMI/FMI比率和生存率之间存在关联，SMI/FMI比率最低的五分位数患者的生存率明显低于最高的五分位数，无论是在粗糙模型中还是在调整年龄、性别和合病后。此外，FMI、放射密度和SMI/FMI与Charlson合并症指数(P <；0.01)。结论SMI/FMI比值可能与移植前合并症和移植后生存有关，尽管SMI的意义尚不清楚。这表明SMI/FMI比值比单独的骨骼肌数量更能反映肌肉损伤。这一发现可能反映了肌肉质量、肌肉脂肪浸润和代谢健康之间复杂的相互作用，这些都是健康和长寿的重要决定因素。总之，我们的研究强调了SMI/FMI比率作为KTx后预后预测因子的潜力，这一发现可能适用于其他患者群体。
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引用次数: 0
Cardiovascular and muscular plasticity in an endurance-master athlete following 12 weeks of detraining and retraining: a case study 一名耐力级运动员经过12周的去训练和再训练后的心血管和肌肉可塑性：一个案例研究
JCSM rapid communications
Pub Date : 2024-05-30 DOI: 10.1002/rco2.93
Nadège Zanou, Vincent Gremeaux, Nicolas Place, Romuald Lepers

Background

This study examined the cardiorespiratory and muscular adaptations of a 53-year-old endurance master athlete following 12 weeks of detraining and retraining.

Methods

Data were collected before and after detraining, and after retraining. Maximal oxygen uptake (VO2max) was evaluated during maximal cycling exercise. Proteins involved in muscle contraction, mitochondrial function and glycolysis were investigated using western blot analysis.

Results

VO2max decreased by 7% after detraining and was 5% greater than baseline after retraining. Detraining induced an important increase in the ryanodine receptor type 1 protein levels (RyR1, +44%) with a decrease in the protein levels of its stabilizer FKBP12 (−24%). We observed a 138% increase in the sarco-endoplasmic reticulum ATPase 1 protein and a 42% increase in the myosin heavy chain fast-twitch protein in response to detraining. This was associated with depressed levels of the mitochondrial biogenesis and oxidative phosphorylation (OXPHOS) proteins, while the expression of the mitochondrial dynamic proteins appeared stimulated. Twelve weeks of retraining reversed almost all the alterations observed in muscle proteins, but specifically increased mitochondrial biogenesis, OXPHOS and antioxidant defence proteins as well as the glucose transporter 4 (Glut-4, +36%) and hexokinase (+100%) proteins levels above the baseline. The mitochondrial dynamic proteins were further increased with the retraining.

Conclusions

These data provide novel information on cardiorespiratory and muscular plasticity, suggesting that highly endurance-trained athletes might show substantial muscular adaptations while retrained after a detraining period and call for more extensive clinical trials.

本研究检测了一名53岁的耐力级运动员在12周的去训练和再训练后的心肺和肌肉适应性。方法收集去训练前后和再训练前后的数据。最大摄氧量（VO2max）在最大循环运动中进行评估。蛋白参与肌肉收缩，线粒体功能和糖酵解用western blot分析。结果去训练后最大摄氧量下降7%，再训练后较基线提高5%。去训练诱导ryanodine受体1型蛋白水平（RyR1, +44%）显著增加，其稳定剂FKBP12蛋白水平下降（- 24%）。我们观察到肌内质网atp酶1蛋白增加138%，肌球蛋白重链快速收缩蛋白增加42%。这与线粒体生物发生和氧化磷酸化（OXPHOS）蛋白水平下降有关，而线粒体动态蛋白的表达则受到刺激。12周的再训练几乎逆转了肌肉蛋白中观察到的所有变化，但特别是线粒体生物发生、OXPHOS和抗氧化防御蛋白以及葡萄糖转运蛋白4（谷氨酸-4，+36%）和己糖激酶（+100%）蛋白水平高于基线水平。随着再训练，线粒体动态蛋白进一步增加。这些数据提供了关于心肺和肌肉可塑性的新信息，表明高耐力训练的运动员可能在去训练期后再训练时表现出大量的肌肉适应性，需要更广泛的临床试验。
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引用次数: 0
Uncorrected and subcutaneous fat-corrected echo intensities are similarly associated with magnetic resonance imaging per cent fat 未校正回波强度和皮下脂肪校正回波强度与磁共振成像脂肪百分比的关系相似
JCSM rapid communications
Pub Date : 2024-05-07 DOI: 10.1002/rco2.92
Benjamin Rush, Sujay Garlapati, Jevin Lortie, Katie Osterbauer, Timothy J. Colgan, Daiki Tamada, Toby C. Campbell, Anne Traynor, Ticiana Leal, Kenneth Lee, Scott B. Reeder, Adam J. Kuchnia

Background

Establishing interchangeable biomedical imaging-based measures to assess myosteatosis clinically may lead to the prevention of muscle wasting, yet neither a consensus measure nor a conversion between measures exists. Ultrasound echo intensity (EI) potentially assesses myosteatosis, but subcutaneous adipose tissue (SAT) thickness and user force application have been shown to influence EI. Although correction factors exist to adjust EI for SAT thickness, they are modelled against poor or no reference measures. Modelling EI corrections against a robust reference measure of myosteatosis, like magnetic resonance imaging (MRI)-based proton density fat fraction (PDFF), is necessary for EI's clinical application.

Methods

Healthy young adults, healthy older adults, and older adults undergoing treatment for lung cancer (n = 10 per group with 50% females) had PDFF and EI at 0, 5, 10, and 15 N measured on their right rectus femoris (RF). We compared EI, SAT thickness, and RF thickness between forces and groups and assessed the relationships between EI adjusted by four different correction factors and PDFF.

Results

The mean age of our sample was 48.63 ± 19.68 years and had a body mass index of 25.21 ± 5.19 kg/m2. The correlation between PDFF and raw EI was r = 0.59 (P < 0.001) with negligible increases by previously published correction factors (Young: 0.62, P < 0.001; Neto Müller: 0.61, P < 0.001). EI, SAT thickness, and RF thickness did not significantly differ between forces (χ2 = 0.31, P = 0.957; χ2 = 2.39, P = 0.496; and χ2 = 7.75, P = 0.051, respectively). EI and PDFF were significantly lower among young healthy adults compared with older adult groups (χ2 = 12.88, P = 0.002, and χ2 = 9.13, P = 0.010, respectively).

Conclusions

EI is correlated with PDFF regardless of force with no improvement from previously published correction factors. Our results suggest that EI is clinically useful and influenced by fat content, yet correction factors must account for more than SAT thickness alone and require further investigation.

背景 建立可互换的基于生物医学成像的临床评估方法来评估肌肉骨质疏松症，可能有助于预防肌肉萎缩，但目前既没有达成共识的方法，也不存在不同方法之间的转换。超声回波强度（EI）可评估肌骨软化症，但已证明皮下脂肪组织（SAT）厚度和使用者施力会影响 EI。尽管存在根据 SAT 厚度调整 EI 的校正因子，但它们都是根据较差的或没有参考测量值的情况建模的。根据可靠的肌骨质疏松症参考指标（如基于磁共振成像（MRI）的质子密度脂肪分数（PDFF））来建立 EI 修正模型，对于 EI 的临床应用非常必要。 方法 对健康的年轻人、健康的老年人和正在接受肺癌治疗的老年人（每组 10 人，女性占 50%）的右股直肌（RF）进行 0、5、10 和 15 N 的质子密度脂肪分数（PDFF）和 EI 测量。我们比较了不同力量和组间的 EI、SAT 厚度和 RF 厚度，并评估了经四种不同校正因子调整的 EI 与 PDFF 之间的关系。 结果 样本的平均年龄为 48.63 ± 19.68 岁，体重指数为 25.21 ± 5.19 kg/m2。PDFF 与原始 EI 之间的相关性为 r = 0.59（P < 0.001），与之前公布的校正因子（Young：0.62，P < 0.001；Neto Müller：0.61，P < 0.001）的相关性几乎可以忽略不计。不同力量之间的 EI、SAT 厚度和 RF 厚度差异不大（分别为 χ2 = 0.31，P = 0.957；χ2 = 2.39，P = 0.496；χ2 = 7.75，P = 0.051）。与老年人组相比，年轻健康成人的 EI 和 PDFF 明显较低（分别为 χ2 = 12.88，P = 0.002 和 χ2 = 9.13，P = 0.010）。 结论 无论力量大小，EI 都与 PDFF 相关，与之前公布的校正因子相比没有改进。我们的结果表明，EI 在临床上是有用的，并受脂肪含量的影响，但校正因子必须比 SAT 厚度单独考虑更多因素，因此需要进一步研究。
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引用次数: 0
A genome wide association study to identify germline copy number variants associated with cancer cachexia: a preliminary analysis 通过基因组全关联研究确定与癌症恶病质相关的种系拷贝数变异：初步分析
JCSM rapid communications
Pub Date : 2024-04-18 DOI: 10.1002/rco2.91
Ashok Narasimhan, Mahalakshmi Kumaran, Ioannis Gioulbasanis, Richard J.E. Skipworth, Oliver F. Bathe, Stein Kaasa, Florian Strasser, Bruno Gagnon, Vickie Baracos, Sambasivarao Damaraju

Background

Cancer cachexia is characterized by severe loss of muscle and fat involving a complex interplay of host–tumour interactions. While much emphasis has been placed on understanding the molecular mechanisms associated with cachexia, understanding the heritable component of cachexia remains less explored. The current study aims to identify copy number variants (CNV) as genetic susceptibility determinants for weight loss in patients with cancer cachexia using genome wide association study (GWAS) approach.

Methods

A total of 174 age-matched patients with oesophagogastric or lung cancer were classified as weight losing (>10% weight loss) or weight stable participants (<2% weight loss). DNA was genotyped using Affymetrix SNP 6.0 arrays to profile CNVs. We tested CNVs with >5% frequency in the population for association with weight loss. Pathway analysis was performed using the genes embedded within CNVs. To understand if the CNVs in the present study are also expressed in skeletal muscle of patients with cachexia, we utilized two publicly available human gene expression datasets to infer the relevance of identified genes in the context of cachexia.

Results

Among the associated CNVs, 5414 CNVs had embedded protein coding genes. Of these, 1583 CNVs were present at >5% frequency. We combined multiple contiguous CNVs within the same genomic region and called them Copy Number Variable Region (CNVR). This led to identifying 896 non-redundant CNV/CNVRs, which encompassed 803 protein coding genes. Genes embedded within CNVs were enriched for several pathways implicated in cachexia and muscle wasting including JAK–STAT signalling, Oncostatin M signalling, Wnt signalling and PI3K-Akt signalling. This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. Further, we show that a subset of CNV/CNVR embedded genes identified in the current study are common with the previously published skeletal muscle gene expression datasets, indicating that expression of CNV/CNVR genes in muscle may have functional consequences in patients with cachexia. These genes include CPT1B, SPON1, LOXL1, NFAT5, RBFOX1, and PCSK6 to name a few.

Conclusions

This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. The data generated will aid in future replication studies in larger cohorts to account for genetic susceptibility to weig

背景癌症恶病质的特点是肌肉和脂肪严重流失，其中涉及宿主与肿瘤之间复杂的相互作用。尽管人们非常重视了解与恶病质相关的分子机制，但对恶病质遗传因素的了解仍然较少。本研究旨在利用全基因组关联研究（GWAS）方法确定拷贝数变异（CNV）作为癌症恶病质患者体重减轻的遗传易感性决定因素。 方法 共有 174 名年龄匹配的食管胃癌或肺癌患者被分为体重减轻者（体重减轻 10%）和体重稳定者（体重减轻 2%）。使用 Affymetrix SNP 6.0 阵列对 DNA 进行基因分型，以确定 CNV。我们测试了人群中频率为 5%的 CNV 与体重减轻的关系。利用嵌入 CNV 的基因进行了通路分析。为了了解本研究中的 CNV 是否也在恶病质患者的骨骼肌中表达，我们利用两个公开的人类基因表达数据集来推断所发现的基因与恶病质的相关性。 结果 在相关的 CNV 中，有 5414 个 CNV 嵌入了蛋白质编码基因。其中，1583 个 CNV 的出现频率为 5%。我们将同一基因组区域内多个连续的 CNVs 合并，称其为拷贝数可变区（CNVR）。这样就确定了 896 个非冗余 CNV/CNVR，其中包括 803 个蛋白质编码基因。嵌入 CNVs 的基因富集于与恶病质和肌肉萎缩有关的几个通路，包括 JAK-STAT 信号、Oncostatin M 信号、Wnt 信号和 PI3K-Akt 信号。这是首个将 CNVs 鉴定为癌症恶病质遗传决定因素的 GWAS 原理验证研究。此外，我们还发现，本研究中发现的一部分 CNV/CNVR 嵌入基因与之前发表的骨骼肌基因表达数据集具有共通性，这表明 CNV/CNVR 基因在肌肉中的表达可能会对恶病质患者产生功能性影响。这些基因包括 CPT1B、SPON1、LOXL1、NFAT5、RBFOX1 和 PCSK6 等。 结论 这是首次将 CNVs 确定为癌症恶病质遗传决定因素的原理性 GWAS 研究。所产生的数据将有助于今后在更大的队列中进行重复研究，以解释癌症恶病质患者体重减轻的遗传易感性。
{"title":"A genome wide association study to identify germline copy number variants associated with cancer cachexia: a preliminary analysis","authors":"Ashok Narasimhan,&nbsp;Mahalakshmi Kumaran,&nbsp;Ioannis Gioulbasanis,&nbsp;Richard J.E. Skipworth,&nbsp;Oliver F. Bathe,&nbsp;Stein Kaasa,&nbsp;Florian Strasser,&nbsp;Bruno Gagnon,&nbsp;Vickie Baracos,&nbsp;Sambasivarao Damaraju","doi":"10.1002/rco2.91","DOIUrl":"https://doi.org/10.1002/rco2.91","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cancer cachexia is characterized by severe loss of muscle and fat involving a complex interplay of host–tumour interactions. While much emphasis has been placed on understanding the molecular mechanisms associated with cachexia, understanding the heritable component of cachexia remains less explored. The current study aims to identify copy number variants (CNV) as genetic susceptibility determinants for weight loss in patients with cancer cachexia using genome wide association study (GWAS) approach.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 174 age-matched patients with oesophagogastric or lung cancer were classified as weight losing (&gt;10% weight loss) or weight stable participants (&lt;2% weight loss). DNA was genotyped using Affymetrix SNP 6.0 arrays to profile CNVs. We tested CNVs with &gt;5% frequency in the population for association with weight loss. Pathway analysis was performed using the genes embedded within CNVs. To understand if the CNVs in the present study are also expressed in skeletal muscle of patients with cachexia, we utilized two publicly available human gene expression datasets to infer the relevance of identified genes in the context of cachexia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the associated CNVs, 5414 CNVs had embedded protein coding genes. Of these, 1583 CNVs were present at &gt;5% frequency. We combined multiple contiguous CNVs within the same genomic region and called them Copy Number Variable Region (CNVR). This led to identifying 896 non-redundant CNV/CNVRs, which encompassed 803 protein coding genes. Genes embedded within CNVs were enriched for several pathways implicated in cachexia and muscle wasting including JAK–STAT signalling, Oncostatin M signalling, Wnt signalling and PI3K-Akt signalling. This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. Further, we show that a subset of CNV/CNVR embedded genes identified in the current study are common with the previously published skeletal muscle gene expression datasets, indicating that expression of CNV/CNVR genes in muscle may have functional consequences in patients with cachexia. These genes include CPT1B, SPON1, LOXL1, NFAT5, RBFOX1, and PCSK6 to name a few.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. The data generated will aid in future replication studies in larger cohorts to account for genetic susceptibility to weig","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"55-65"},"PeriodicalIF":0.0,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.91","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Combined orchiectomy and limb immobilization recapitulate early age-related changes to skeletal muscle in mice 睾丸切除术和肢体固定相结合再现了小鼠骨骼肌早期与年龄有关的变化
JCSM rapid communications
Pub Date : 2024-04-16 DOI: 10.1002/rco2.90
Danielle A. Debruin, Jasmaine Murphy, Dean G. Campelj, Ryan Bagaric, Cara A. Timpani, Craig A. Goodman, Erik D. Hanson, Emma Rybalka, Alan Hayes

Background

Muscle mass and function decline in middle age, ultimately resulting in sarcopenia in the elderly and poor health outcomes, reducing quality of life. There is a lack of cost- and time-effective murine models that recapitulate the physiological changes associated with muscle mass decline to study possible interventions to delay sarcopenia. We aimed to evaluate the effectiveness of combining orchiectomy (ORC) surgery to simulate age-related androgen decline and hindlimb immobilization (IM) in inducing age-related skeletal muscle changes.

Methods

Four-month-old male C57BL/6J mice (n = 10) were subjected to ORC, followed by IM (right hindlimb casting) for 14 days. Upon completion of the casting period, ex vivo muscle contractile function, histology, and various mitochondrial markers were assessed, and results were compared with age-matched controls (CON; n = 8) and middle-aged (MA; 12 ± 1 months, n = 9) animals.

Results

IM combined with ORC induced a 30%–40% decrease in muscle mass across multiple hindlimb muscles (P < 0.0001), with the magnitude of muscle loss comparable with the MA group when corrected for body weight (P < 0.0001). In the IM limb of ORC mice, soleus muscle force significantly decreased when compared with the contralateral limb (P < 0.05) and aged-matched CON group (P < 0.05). The decrements in muscle force and mass present in the IM limb of ORC mice were accompanied by a 70% reduction in the expression of the muscle structural protein dystrophin and various mitochondrial markers, including cytochrome C (−55%), peroxisome proliferator-activated receptor gamma co-activator 1-beta (PGC1-β) (−49%), and cytochrome oxidase IV (COX-IV) (−73%) when compared with CON animals (P < 0.001). Lastly, our model also demonstrated specific fibre-type shifts in fast- and slow-twitch muscles, which mimicked changes in the MA group.

Conclusions

Applying treatments during IM could target acute muscle atrophy in MA adults, while applying them following cast removal in a low-testosterone environment could represent a window for rehabilitation therapeutics.

背景 肌肉质量和功能在中年时会下降，最终导致老年人肌肉疏松症和不良的健康状况，降低生活质量。目前缺乏成本低、时间短、效果好的小鼠模型来再现肌肉质量下降的相关生理变化，从而研究延缓肌肉疏松症的可能干预措施。我们旨在评估睾丸切除手术（ORC）模拟与年龄相关的雄激素下降和后肢固定（IM）在诱导与年龄相关的骨骼肌变化方面的有效性。 方法 对四个月大的雄性 C57BL/6J 小鼠（n = 10）进行睾丸切除手术，然后进行为期 14 天的右后肢固定。铸造期结束后，评估体内外肌肉收缩功能、组织学和各种线粒体标记物，并将结果与年龄匹配的对照组（CON；n = 8）和中年组（MA；12 ± 1 个月，n = 9）动物进行比较。 结果 IM 与 ORC 联用会导致后肢多块肌肉的肌肉质量下降 30%-40%（P < 0.0001），根据体重校正后，肌肉损失的程度与 MA 组相当（P < 0.0001）。与对侧肢体（P <0.05）和年龄匹配的CON组（P <0.05）相比，ORC小鼠IM肢体的比目鱼肌力显著下降。与对照组相比，ORC 小鼠肢体肌力和肌肉质量下降的同时，肌肉结构蛋白肌营养不良蛋白和各种线粒体标记物的表达也减少了 70%，其中包括细胞色素 C（-55%）、过氧化物酶体增殖激活受体伽马共激活因子 1-β（PGC1-β）（-49%）和细胞色素氧化酶 IV（COX-IV）（-73%）（P < 0.001）。最后，我们的模型还显示了快慢肌特定纤维类型的变化，这与 MA 组的变化相似。 结论 在 IM 期间应用治疗方法可针对 MA 成年人的急性肌肉萎缩，而在低睾酮环境中拆除石膏后应用治疗方法可代表康复疗法的一个窗口。
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引用次数: 0
Betulinic acid ameliorates cast-immobilized skeletal muscle atrophy but not denervation-induced skeletal muscle atrophy 白桦脂酸可改善石膏固定的骨骼肌萎缩，但不能改善去神经诱导的骨骼肌萎缩
JCSM rapid communications
Pub Date : 2024-04-01 DOI: 10.1002/rco2.89
Yuki Enoki, Yuki Kanezaki, Isamu Takahata, Kazuaki Taguchi, Kazuaki Matsumoto

Background

Terpenoids have gained attention as therapeutic agents for skeletal muscle atrophy owing to their various physiological activities. In this study, we screened four terpenoids for their therapeutic potential against muscle atrophy in cultured cells and evaluated the effectiveness of betulinic acid in two disuse muscle atrophy models.

Methods

C2C12 cells were used as the skeletal muscle model in cell culture experiments. Betulinic acid (100 mg/kg, twice daily) was administered to two different mouse models of muscle atrophy (established using the sciatic denervation and casting methods) for 7 days.

Results

In myotube experiments, the mRNA expression of atrogin-1 and myostatin was significantly suppressed by betulinic and ursolic acids (P < 0.05). In the differentiation phase of C2C12 myotubes, the mRNA expression levels of myoD and myogenin were significantly increased by betulinic acid (P < 0.05). In addition, apelin and irisin were also significantly increased by betulinic acid (P < 0.05 and 0.01, respectively). Consequently, betulinic acid was administered to the aforementioned muscle atrophy models. Betulinic acid did not inhibit the decrease in skeletal muscle weight observed in the denervation model. However, it significantly inhibited the decrease in tibialis anterior (TA) and extensor digitorum longus (EDL) weights and grip strength observed in the cast-immobilized skeletal muscle atrophy model (TA: Cast + Veh vs. Cast + Bet = 42.6 ± 1.0 vs. 46.0 ± 0.8 mg, P < 0.01; EDL: Cast + Veh vs. Cast + Bet = 9.0 ± 0.4 vs. 11.3 ± 0.5 mg, P < 0.01; grip strength: Cast + Veh vs. Cast + Bet = 222 ± 4.8 vs. 245 ± 3.6 g, P < 0.05). In addition, betulinic acid administration partially inhibited the decrease in skeletal muscle cross-sectional area.

Conclusions

Betulinic acid alleviated muscle atrophy in the cast model of muscle atrophy and has therapeutic potential for the treatment of immobilized disuse skeletal muscle atrophy.

背景 萜类化合物具有多种生理活性，因此作为骨骼肌萎缩的治疗药物已受到关注。本研究筛选了四种萜类化合物在培养细胞中对肌肉萎缩的治疗潜力，并评估了白桦脂酸在两种废用性肌肉萎缩模型中的有效性。 方法 在细胞培养实验中使用 C2C12 细胞作为骨骼肌模型。给两种不同的肌肉萎缩小鼠模型（使用坐骨神经去神经和铸造法建立）注射白桦脂酸（100 毫克/千克，每天两次），为期 7 天。 结果 在肌管实验中，白桦脂酸和熊果酸显著抑制了atrogin-1和myostatin的mRNA表达（P< 0.05）。在 C2C12 肌管的分化阶段，桦木酸可明显提高 myoD 和 myogenin 的 mRNA 表达水平（P < 0.05）。此外，凋亡素和鸢尾素也在白桦脂酸的作用下明显增加（P分别为0.05和0.01）。因此，将白桦脂酸用于上述肌肉萎缩模型。白桦脂酸不能抑制去神经模型中观察到的骨骼肌重量的减少。然而，白桦脂酸却能明显抑制在石膏固定骨骼肌萎缩模型中观察到的胫骨前肌（TA）和趾长伸肌（EDL）重量和握力的下降（TA：Cast + Veh vs. EDL：Cast + Bet = 42.6 ± 2.5 ± 2.5）。铸塑 + Bet = 42.6 ± 1.0 vs. 46.0 ± 0.8 mg，P < 0.01；EDL：铸塑 + Veh vs. 铸塑 + Bet = 9.0 ± 0.4 vs. 11.3 ± 0.5 mg，P < 0.01；握力：铸塑 + Veh vs. 铸塑 + Bet = 9.0 ± 0.4 vs. 11.3 ± 0.5 mg，P < 0.01）：Cast + Veh vs. Cast + Bet = 222 ± 4.8 vs. 245 ± 3.6 g，P < 0.05）。此外，白桦脂酸还能部分抑制骨骼肌横截面积的减少。 结论 白桦脂酸可缓解石膏模型肌肉萎缩，具有治疗固定失用性骨骼肌萎缩的潜力。
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引用次数: 0
Publication trends and hot spots in the Journal of Cachexia, Sarcopenia and Muscle: A bibliometric analysis (2010–2022) 痛症、肌肉疏松症与肌肉杂志》的出版趋势与热点：文献计量分析（2010-2022 年）
JCSM rapid communications
Pub Date : 2024-02-29 DOI: 10.1002/rco2.88
Dong-liang Yuan, Wen-qing Xie, Miao He, Deng-jie Yu, Heng-zhen Li, Hong-fu Jin, Guang Yang, Bing-zhou Ji, Wen-feng Xiao, Yu-sheng Li

Background

The Journal of Cachexia, Sarcopenia and Muscle is a quarterly peer-reviewed medical journal published by WILEY since 2010 and has been dedicated to advancing research on chronic diseases, especially cachexia and sarcopenia. Over the past 12 years, sarcopenia research worldwide has significantly changed. This study aimed to investigate different aspects of studies published in this journal.

Methods

Using the term ‘Journal of Cachexia, Sarcopenia and Muscle’, we retrieved related publications from the Web of Science and PubMed databases. Studies published in this journal were classified and analysed from different perspectives, such as the number of studies, total citations, times cited per item, H-index, research area, article types, institutions, country and funding agency. The VOS viewer software was used for co-occurrence, bibliographic coupling, co-citation and co-authorship analyses.

Results

From 2010 to 2022, 1194 studies were published in the Journal of Cachexia, Sarcopenia and Muscle. The United States was the highest contributor, with the most publications and citations and the highest H-index. Italy ranked first for the times cited per item. The main research area was geriatrics and gerontology. von Haehling S was the author with the highest impact. The National Institutes of Health, USA, and the United States Department of Health Human Services funded the maximum number of studies. The top 5 most frequently used keywords in all publications over 12 years were sarcopenia, cachexia, skeletal muscle, body composition and muscle mass. The Journal of Cachexia, Sarcopenia and Muscle was cited the most by Nutrients, and PLOS ONE was cited the most by the Journal of Cachexia, Sarcopenia and Muscle.

Conclusions

Publications in the Journal of Cachexia, Sarcopenia and Muscle have significantly increased from 2010 to 2022, especially in recent years. The United States is still the leader in sarcopenia research. Future submissions to this journal will continue to focus on sarcopenia, cachexia, skeletal muscle, body-composition and muscle mass. The aetiology, molecular mechanisms and outcomes of sarcopenia and cachexia are current research hotspots.

背景 《恶病质、肌肉疏松症与肌肉杂志》是由 WILEY 于 2010 年出版的同行评审医学季刊，一直致力于推动慢性疾病，尤其是恶病质和肌肉疏松症的研究。在过去的 12 年中，全球范围内的肌肉疏松症研究发生了重大变化。本研究旨在调查在该期刊上发表的研究的各个方面。 方法 我们以 "Journal of Cachexia, Sarcopenia and Muscle "为关键词，从 Web of Science 和 PubMed 数据库中检索了相关出版物。我们从研究数量、总引用次数、每项被引次数、H 指数、研究领域、文章类型、机构、国家和资助机构等不同角度对发表在该期刊上的研究进行了分类和分析。使用 VOS 浏览器软件进行共现、书目耦合、共引和合著分析。 结果 从 2010 年到 2022 年，《痛症、肉质疏松症和肌肉杂志》共发表了 1194 篇研究论文。美国是贡献最多的国家，发表的论文最多，被引用的次数最多，H 指数也最高。意大利的单篇引用次数排名第一。von Haehling S 是影响最大的作者。美国国立卫生研究院和美国卫生人类服务部资助的研究数量最多。12 年来，所有出版物中使用频率最高的 5 个关键词是肌肉疏松症、恶病质、骨骼肌、身体成分和肌肉质量。营养素》对《恶病质、肌肉减少症与肌肉杂志》的引用率最高，而《PLOS ONE》对《恶病质、肌肉减少症与肌肉杂志》的引用率最高。 结论 从2010年到2022年，《痛症、肌肉疏松症与肌肉杂志》上的论文数量显著增加，尤其是近年来。美国在肌肉疏松症研究方面仍处于领先地位。本期刊今后的投稿将继续关注肌肉疏松症、恶病质、骨骼肌、身体结构和肌肉质量。肌肉疏松症和恶病质的病因、分子机制和结果是当前的研究热点。
{"title":"Publication trends and hot spots in the Journal of Cachexia, Sarcopenia and Muscle: A bibliometric analysis (2010–2022)","authors":"Dong-liang Yuan,&nbsp;Wen-qing Xie,&nbsp;Miao He,&nbsp;Deng-jie Yu,&nbsp;Heng-zhen Li,&nbsp;Hong-fu Jin,&nbsp;Guang Yang,&nbsp;Bing-zhou Ji,&nbsp;Wen-feng Xiao,&nbsp;Yu-sheng Li","doi":"10.1002/rco2.88","DOIUrl":"https://doi.org/10.1002/rco2.88","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The <i>Journal of Cachexia, Sarcopenia and Muscle</i> is a quarterly peer-reviewed medical journal published by WILEY since 2010 and has been dedicated to advancing research on chronic diseases, especially cachexia and sarcopenia. Over the past 12 years, sarcopenia research worldwide has significantly changed. This study aimed to investigate different aspects of studies published in this journal.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using the term ‘Journal of Cachexia, Sarcopenia and Muscle’, we retrieved related publications from the Web of Science and PubMed databases. Studies published in this journal were classified and analysed from different perspectives, such as the number of studies, total citations, times cited per item, H-index, research area, article types, institutions, country and funding agency. The VOS viewer software was used for co-occurrence, bibliographic coupling, co-citation and co-authorship analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>From 2010 to 2022, 1194 studies were published in the <i>Journal of Cachexia, Sarcopenia and Muscle</i>. The United States was the highest contributor, with the most publications and citations and the highest H-index. Italy ranked first for the times cited per item. The main research area was geriatrics and gerontology. von Haehling S was the author with the highest impact. The National Institutes of Health, USA, and the United States Department of Health Human Services funded the maximum number of studies. The top 5 most frequently used keywords in all publications over 12 years were sarcopenia, cachexia, skeletal muscle, body composition and muscle mass. The <i>Journal of Cachexia, Sarcopenia and Muscle</i> was cited the most by <i>Nutrients</i>, and PLOS ONE was cited the most by the <i>Journal of Cachexia, Sarcopenia and Muscle</i>.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Publications in the <i>Journal of Cachexia, Sarcopenia and Muscle</i> have significantly increased from 2010 to 2022, especially in recent years. The United States is still the leader in sarcopenia research. Future submissions to this journal will continue to focus on sarcopenia, cachexia, skeletal muscle, body-composition and muscle mass. The aetiology, molecular mechanisms and outcomes of sarcopenia and cachexia are current research hotspots.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"17-29"},"PeriodicalIF":0.0,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.88","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141453593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hypoxia-inducible factor prolyl hydroxylase domain inhibitors may mitigate loss of skeletal muscle mass in haemodialysis patients 缺氧诱导因子脯氨酰羟化酶结构域抑制剂可减轻血液透析患者骨骼肌质量的损失
JCSM rapid communications
Pub Date : 2024-01-04 DOI: 10.1002/rco2.87
Hiroko Hashimoto, Shintaro Mandai, Satomi Shikuma, Mai Kimura, Hayato Toma, Yuki Sakaguchi, Moe Kimura, Jun Ota, Yoshihiko Chiba, Keigo Sakai, Susumu Horiuchi, Susumu Adachi, Shinichi Uchida

Background

Chronic kidney disease patients particularly with renal anaemia hyporesponsive to erythropoiesis-stimulating agents (ESAs) are at a greater risk of having skeletal muscle mass (SMM) loss. Hypoxia-inducible factor prolyl hydroxylase domain inhibitor (HIF-PHI), a novel therapeutic agent for renal anaemia, potentially promotes angiogenesis, muscle repair, and homeostasis. However, effects of HIF-PHIs on SMM remain unknown.

Methods

This retrospective observational cohort study enrolled 292 Japanese adults receiving maintenance haemodialysis at our dialysis centre. The dataset included 11 patients who received daprodustat for 6 months or longer during 1 December 2020 through 30 June 2022. From the previously published pooled cohort, we enrolled 281 participants from 1 August 2018 to 31 July 2019 prior to the approval of HIF-PHIs for renal anaemia. SMM was assessed using modified creatinine index (mg/kg/day) calculated by age, sex, serum creatinine, and single-pool Kt/V. Annual changes of SMM [ΔSMM (%)] were analysed with the least squares regression model and mixed-effects model during 6- to 12-month follow-up period.

Results

The median age of the participants was 63 years [interquartile range (IQR), 54–71 years], and 33% were female. The median ΔSMM levels (IQR) in the least squares regression model were 4.0% (−1.7% to 9.3%) in the HIF-PHI group, 0.20% (−2.1% to 2.1%) in the no ESA group, and −0.94% (−3.0% to 1.3%) in the high ESA group using darbepoetin equivalent to 20 μg or more per week. Those in the mixed-effects model were −1.7% (−1.2% to 3.8%), 0.09% (−1.4% to 1.3%), and −0.74% (−2.0% to 0.8%), respectively. The multivariable linear regression models revealed that HIF-PHI use was associated with greater ΔSMM compared with the high ESA group [coefficient, 3.737; 95% confidence interval (CI), 1.216–6.258 in the least squares regression model or coefficient, 1.635; 95% CI, 0.068–3.201 in the mixed-effects model, respectively].

Conclusions

HIF-PHI use led to greater ΔSMM in maintenance haemodialysis patients. HIF-PHIs may minimize loss of SMM in patients with end-stage kidney disease and renal anaemia.

慢性肾病患者，尤其是对促红细胞生成药（ESAs）反应迟钝的肾性贫血患者，骨骼肌质量（SMM）下降的风险更大。缺氧诱导因子脯氨酰羟化酶结构域抑制剂（HIF-PHI）是一种治疗肾性贫血的新型药物，可促进血管生成、肌肉修复和平衡。然而，HIF-PHIs 对 SMM 的影响仍然未知。这项回顾性观察队列研究纳入了 292 名在我们的透析中心接受维持性血液透析的日本成年人。数据集包括在 2020 年 12 月 1 日至 2022 年 6 月 30 日期间接受达泊司他（daprodustat）治疗 6 个月或更长时间的 11 名患者。从之前发表的汇集队列中，我们在肾性贫血 HIF-PHIs 批准之前的 2018 年 8 月 1 日至 2019 年 7 月 31 日期间招募了 281 名参与者。SMM采用按年龄、性别、血清肌酐和单池Kt/V计算的改良肌酐指数（毫克/千克/天）进行评估。在 6 至 12 个月的随访期间，采用最小二乘法回归模型和混合效应模型分析了 SMM 的年度变化[ΔSMM (%)]。在最小二乘法回归模型中，HIF-PHI组的中位ΔSMM水平（IQR）为4.0%（-1.7%至9.3%），无ESA组为0.20%（-2.1%至2.1%），每周使用相当于20微克或更多达贝泊汀的高ESA组为-0.94%（-3.0%至1.3%）。在混合效应模型中，这一比例分别为-1.7%（-1.2%至3.8%）、0.09%（-1.4%至1.3%）和-0.74%（-2.0%至0.8%）。多变量线性回归模型显示，与高ESA组相比，使用HIF-PHI与更大的ΔSMM相关[最小二乘回归模型中的系数为3.737；95%置信区间（CI）为1.216-6.258，混合效应模型中的系数为1.635；95%置信区间（CI）为0.068-3.201]。HIF-PHI可最大限度地减少终末期肾病和肾性贫血患者的SMM损失。
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引用次数: 0
The role of microRNAs in critical illness—do miRs truly ‘miRror’ muscle wasting? microRNA 在危重病中的作用--miRs 真的能 "miRror "肌肉萎缩吗？
JCSM rapid communications
Pub Date : 2023-12-26 DOI: 10.1002/rco2.86
Ryosuke Sato, Stephan von Haehling
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引用次数: 0
Molecular changes in skeletal muscle in chronic kidney disease: A systematic review 慢性肾脏病骨骼肌的分子变化：系统综述
JCSM rapid communications
Pub Date : 2023-12-26 DOI: 10.1002/rco2.82
Limy Wong, Rachel Kenny, Jennifer Howard, Lawrence P. McMahon

Background

Loss of skeletal muscle mass is prevalent among patients affected by chronic kidney disease (CKD). It is associated with significant morbidity and mortality. The underlying molecular pathogenesis has yet to be fully understood. The aim of this systematic review is to summarize the current evidence on molecular changes in the skeletal muscle of humans and rodents with CKD and to assess the strength of such evidence.

Methods

The PubMed and EMBASE databases were searched using three main themes: messenger ribonucleic acid/protein/microRNA expression, skeletal muscle and CKD. This study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards.

Results

A total of 98 studies were included in the systematic review, comprising 26 prospective human clinical studies, four human and rodent studies, and 68 rodent-only studies (32 mouse and 36 rat models respectively). The sample sizes of human studies were largely small (40% of studies had ≤20 participants). Qualitative polymerase chain reaction (qPCR) was the most commonly used method for gene expression and none of the studies fulfilled the Minimum Information for Publication of qPCR Experiments criteria for quality assessment. Majority of the studies investigated only a few genes or a specific signalling pathway. FBXO32, TRIM63, MSTN, IL6, TNF and IGF1 were the most investigated genes. The identified differentially expressed genes and proteins belonged to eight major pathways, including apoptosis, autophagy, inflammation, insulin/insulin-like growth factor 1 signalling, lipid metabolism, mitochondrial function, muscle cell growth and differentiation, and protein degradation, similar to other chronic disease states.

Conclusions

The current evidence regarding molecular alterations in the skeletal muscle in CKD is largely derived from small and heterogenous studies. Markedly similar modifications in the major biological pathways between CKD and other chronic diseases supports shared deleterious molecular mechanisms producing muscle atrophy, irrespective of the underlying specific disease.

背景 慢性肾脏病（CKD）患者普遍存在骨骼肌质量下降的问题。它与严重的发病率和死亡率有关。其潜在的分子发病机制尚未完全明了。本系统综述旨在总结目前有关 CKD 患者和啮齿类动物骨骼肌分子变化的证据，并评估这些证据的强度。 方法 使用三个主题对 PubMed 和 EMBASE 数据库进行检索：信使核糖核酸/蛋白质/microRNA 表达、骨骼肌和 CKD。本研究按照系统综述和荟萃分析首选报告项目（PRISMA）标准进行。 结果 总共有 98 项研究被纳入系统综述，其中包括 26 项前瞻性人类临床研究、4 项人类和啮齿动物研究以及 68 项纯啮齿动物研究（分别为 32 个小鼠模型和 36 个大鼠模型）。人类研究的样本量大多较小（40% 的研究参与者少于 20 人）。定性聚合酶链反应（qPCR）是最常用的基因表达方法，但没有一项研究符合《qPCR 实验发表最低信息量》的质量评估标准。大多数研究只调查了几个基因或特定的信号通路。FBXO32、TRIM63、MSTN、IL6、TNF 和 IGF1 是调查最多的基因。已确定的差异表达基因和蛋白质属于八种主要通路，包括细胞凋亡、自噬、炎症、胰岛素/胰岛素样生长因子 1 信号传导、脂质代谢、线粒体功能、肌肉细胞生长和分化以及蛋白质降解，这与其他慢性疾病状态类似。 结论 目前有关慢性肾脏病患者骨骼肌分子改变的证据主要来自小型和异质性研究。CKD 和其他慢性疾病的主要生物通路发生了明显的相似变化，这支持了产生肌肉萎缩的共同有害分子机制，而与潜在的特定疾病无关。
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