Skeletal muscle atrophy in clinical and preclinical models of chronic kidney disease: A systematic review and meta-analysis.

Skeletal muscle atrophy in clinical and preclinical models of chronic kidney disease: A systematic review and meta-analysis.
复制标题

DOI:
10.1002/jcsm.13400
复制
发表时间:
2024-02
期刊:
Journal of cachexia, sarcopenia and muscle
影响因子:
--
通讯作者:
--
中科院分区:
其他
文献类型:
--
作者:

文献摘要

参考文献

相似文献

慢性肾脏疾病(CKD)患者通常被认为是肌肉质量的浪费和肌肉力量和功能的下降,统称为肌肉减少症。临床和临床前CKD人群中骨骼肌萎缩的程度尚不清楚。我们评估了CKD临床前和临床模型中的骨骼肌萎缩,对肌肉质量评估方法、CKD严重程度、性别和不同的CKD临床前模型进行了多个子分析。我们对使用以下数据库测量肌肉质量/大小的临床和临床前研究进行了系统性文献综述:奥维德Medline、Embase和Scopus。使用随机效应荟萃分析确定健康和CKD之间的标准平均差(SMD; Hedges 'g)。使用I2统计量评估异质性。通过实验动物实验系统评价中心评估临床前研究质量,通过纽卡斯尔-渥太华量表评估临床研究质量。本研究在检索开始前已在PROSPERO(CRD 42020180737)中注册。本分析共纳入111项研究,分为以下亚组:主要CKD分析中的106项研究、18项糖尿病研究和7项肾移植研究。在78%的临床前研究和49%的临床研究中证实了显著萎缩。随机效应模型显示,总体SMD为中等(SMD = 0.58,95% CI = 0.52 - 0.64)当结合临床和临床前研究时,临床人群的中等SMD(SMD = 0.48,95% CI = 0.42 - 0.55;所有分期)和临床前CKD的大SMD(SMD = 0.95,95% CI = 0.76 - 1.14)。根据评估方法、疾病状态和动物模型进行进一步的子分析。49%的临床研究报告了肌肉萎缩,平均差异较小。临床前研究报告了78%的研究中的显著萎缩,平均差异较大。在多项临床子分析(如CKD严重程度、透析方式和糖尿病)中,发现了中等平均差异。临床和临床前研究的子分析发现,男性的平均差异较大,女性的平均差异中等,表明性别特异性影响。肌肉萎缩差异因临床和临床前研究的评估方法而异。研究设计的局限性使得无法得出关于疾病进展时肌肉损失程度或透析影响的结论。未来的工作将受益于使用标准化的测量方法和一致的临床分期,以提高我们对CKD进展中萎缩变化的理解,并分析生物学性别差异。
Patients with chronic kidney disease (CKD) are often regarded as experiencing wasting of muscle mass and declining muscle strength and function, collectively termed sarcopenia. The extent of skeletal muscle wasting in clinical and preclinical CKD populations is unclear. We evaluated skeletal muscle atrophy in preclinical and clinical models of CKD, with multiple sub‐analyses for muscle mass assessment methods, CKD severity, sex and across the different preclinical models of CKD. We performed a systematic literature review of clinical and preclinical studies that measured muscle mass/size using the following databases: Ovid Medline, Embase and Scopus. A random effects meta‐analysis was utilized to determine standard mean difference (SMD; Hedges' g) between healthy and CKD. Heterogeneity was evaluated using the I 2 statistic. Preclinical study quality was assessed via the Systematic Review Centre for Laboratory Animal Experimentation and clinical studies quality was assessed via the Newcastle‐Ottawa Scale. This study was registered in PROSPERO (CRD42020180737) prior to initiation of the search. A total of 111 studies were included in this analysis using the following subgroups: 106 studies in the primary CKD analysis, 18 studies that accounted for diabetes and 7 kidney transplant studies. Significant atrophy was demonstrated in 78% of the preclinical studies and 49% of the clinical studies. The random effects model demonstrated a medium overall SMD (SMD = 0.58, 95% CI = 0.52–0.64) when combining clinical and preclinical studies, a medium SMD for the clinical population (SMD = 0.48, 95% CI = 0.42–0.55; all stages) and a large SMD for preclinical CKD (SMD = 0.95, 95% CI = 0.76–1.14). Further sub‐analyses were performed based upon assessment methods, disease status and animal model. Muscle atrophy was reported in 49% of the clinical studies, paired with small mean differences. Preclinical studies reported significant atrophy in 78% of studies, with large mean differences. Across multiple clinical sub‐analyses such as severity of CKD, dialysis modality and diabetes, a medium mean difference was found. Sub‐analyses in both clinical and preclinical studies found a large mean difference for males and medium for females suggesting sex‐specific implications. Muscle atrophy differences varied based upon assessment method for clinical and preclinical studies. Limitations in study design prevented conclusions to be made about the extent of muscle loss with disease progression, or the impact of dialysis. Future work would benefit from the use of standardized measurement methods and consistent clinical staging to improve our understanding of atrophy changes in CKD progression, and analysis of biological sex differences.
降低甲酰基-COA去饱和酶(SCD)通过慢性肾脏疾病中过量的内质网应激造成肌肉萎缩。
DOI: 10.3164/jcbn.20-24
发表时间: 2020-09
影响因子: 2.4
作者:
Niida Y;Masuda M;Adachi Y;Yoshizawa A;Ohminami H;Mori Y;Ohnishi K;Yamanaka-Okumura H;Uchida T;Nikawa T;Yamamoto H;Miyazaki M;Taketani Y
通讯作者: Taketani Y
DOI: 10.1038/s41598-021-94565-y
发表时间: 2021-07-23
期刊: Scientific reports
影响因子: 4.6
作者:
Cheung WW;Zheng R;Hao S;Wang Z;Gonzalez A;Zhou P;Hoffman HM;Mak RH
通讯作者: Mak RH
DOI: 10.1038/s41598-019-52107-7
发表时间: 2019-10-29
期刊: SCIENTIFIC REPORTS
影响因子: 4.6
作者:
Berru, Fabian N.;Gray, Sarah E.;Ryan, Terence E.
通讯作者: Ryan, Terence E.
DOI: 10.1152/japplphysiol.00957.2015
发表时间: 2016-05-01
影响因子: 3.3
作者:
Acevedo, Luz M.;Lopez, Ignacio;Rivero, Jose-Luis L.
通讯作者: Rivero, Jose-Luis L.
DOI: 10.1038/ki.1996.160
发表时间: 1996-04-01
影响因子: 19.6
作者:
Fisch, BJ;Spiegel, DM
通讯作者: Spiegel, DM