Shared and distinct mechanisms of skeletal muscle atrophy: A narrative review.
Shared and distinct mechanisms of skeletal muscle atrophy: A narrative review.
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DOI：
10.1016/j.arr.2021.101463
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发表时间：
2021-11
影响因子：
13.1
通讯作者：
Koutakis P
中科院分区：
文献类型：
--
作者：
Wilburn D;Ismaeel A;Machek S;Fletcher E;Koutakis P
骨骼肌质量和功能的维持是合成代谢和分解代谢的微妙平衡，在不同的病理条件下会被扭曲。在本文中，我们打算讨论不同的细胞内信号事件，调节肌肉蛋白萎缩的一个给定的临床发生。除了肌肉退化的常见结果外，有几种情况至少有一种或多种不同的机制，这些机制创造了促进肌肉损失的独特细胞内环境。这些病理的微妙个性可以为研究人员和临床医生提供具体的目标，以进一步确定和提高医学治疗和干预的效果。上图显示了调节骨骼肌合成代谢和分解代谢的不同信号通路。局灶黏附激酶（FAK）通过磷脂酰肌醇3激酶（PI3K）、蛋白激酶B （AKT）途径激活哺乳动物雷帕霉素靶蛋白（mTOR），以响应机械负荷。胰岛素或胰岛素样生长因子（IGF）刺激可以通过同样的级联激活mTOR。还显示了与炎症细胞因子如肿瘤坏死因子-α (TNF-α)和白细胞介素-6 （IL-6）相关的分解代谢途径。TNF-α受体1 （TNFR1）配体结合激活活化B细胞（NF-kB）和c-Jun n-末端激酶（JNK）途径的核因子kappa-轻链增强子，提高蛋白水解率。蛋白激酶R （PKR）也能刺激NF-kB的活化。IL-6受体结合激活Janus激酶（JAK）信号转导器和转录激活因子（STAT）信号，可增加肌肉损失率。转化生长因子- β (TGF- β)受体结合促进小母鼠抗十肢截瘫（SMAD）同源物2和3 （SMAD2/3）磷酸化，以及随后的smad4磷酸化，上调胶原合成和纤维化相关基因。此外，糖皮质激素（GC）受体激活、二聚化和DNA结合随后促进FOXO表达的增加，从而增加UPS相关E3连接酶的表达。在低能量可用性时，增加的5 '腺苷单磷酸活化蛋白激酶(AMPK)- Unc-51样自噬激活激酶1 （ULK1）磷酸化诱导自噬相关过程的激活。
Maintenance of skeletal muscle mass and function is an incredibly nuanced balance of anabolism and catabolism that can become distorted within different pathological conditions. In this paper we intend to discuss the distinct intracellular signaling events that regulate muscle protein atrophy for a given clinical occurrence. Aside from the common outcome of muscle deterioration, several conditions have at least one or more distinct mechanisms that creates unique intracellular environments that facilitate muscle loss. The subtle individuality to each of these given pathologies can provide both researchers and clinicians with specific targets of interest to further identify and increase the efficacy of medical treatments and interventions. Above shows varying signaling pathways that regulate both skeletal muscle anabolism and catabolism. Focal Adhesion Kinase (FAK) is shown activate mammalian target of rapamycin (mTOR) in response to mechanical load through the phosphatidylinositol 3 kinase (PI3K), protein kinase B (AKT) pathway. Insulin or insulin-like growth factor (IGF) stimulation can activate mTOR through the same cascade. Also shown are the catabolic pathways related to inflammatory cytokines such as tumor necrosis factor-α (TNF-α), and interlukin-6 (IL-6). TNF-α receptor 1 (TNFR1) ligand binding activates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and c-Jun N-terminal kinase (JNK) pathway increasing rates of proteolysis. Protein Kinase R (PKR) can also stimulate the activation of NF-kB. IL-6 receptor binding activates the Janus Kinase (JAK) Signal Transducer and Activator of Transcription (STAT) signaling that can increase rates of muscle loss. Transforming Growth Factor-beta (TGF- β) receptor binding facilitates small mothers against decapentaplegic (SMAD) homologs 2 and 3 (SMAD2/3) phosphorylation, and subsequent SMAD 4 phosphorylation, upregulating genes related to collagen synthesis and fibrosis. Additionally, glucocorticoid (GC) receptor activation, dimerization, and DNA binding subsequently facilitates increases in FOXO expression which can increase the expression of UPS related E3 ligases. During low energy availability, increased 5’ adenosine monophosphate-activated protein kinase (AMPK)- Unc-51 like autophagy activating kinase 1 (ULK1) phosphorylation induces the activation of autophagy related processes.
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Sulforaphane通过NRF2信号传导可防止与年龄相关的心脏和肌肉功能障碍。
影响因子：
7.8
作者：
Bose C;Alves I;Singh P;Palade PT;Carvalho E;Børsheim E;Jun SR;Cheema A;Boerma M;Awasthi S;Singh SP
通讯作者：
Singh SP
DOI：
10.3109/08977194.2011.595714
发表时间：
2011-10
期刊：
Growth factors (Chur, Switzerland)
影响因子：
--
作者：
Biernacka A;Dobaczewski M;Frangogiannis NG
通讯作者：
Frangogiannis NG
影响因子：
4.8
作者：
Altun, Mikael;Besche, Henrike C.;Ulfhake, Brun
通讯作者：
Ulfhake, Brun
影响因子：
3.3
作者：
Baehr, Leslie M.;West, Daniel W. D.;Bodine, Sue C.
通讯作者：
Bodine, Sue C.
影响因子：
5.6
作者：
Biagetti B;Simó R
通讯作者：
Simó R