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Impacts of altered exercise volume, intensity, and duration on the activation of AMPK and CaMKII and increases in PGC-1α mRNA 改变运动量、强度和持续时间对AMPK和CaMKII的激活以及PGC-1α mRNA的增加的影响
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2022.05.016
Brendon J. Gurd , Eveline Soares Menezes , Benjamin B. Arhen , Hashim Islam

The purpose of this review is to explore and discuss the impacts of augmented training volume, intensity, and duration on the phosphorylation/activation of key signaling protein – AMPK, CaMKII and PGC-1α - involved in the initiation of mitochondrial biogenesis. Specifically, we explore the impacts of augmented exercise protocols on AMP/ADP and Ca2+ signaling and changes in post exercise PGC − 1α gene expression. Although AMP/ADP concentrations appear to increase with increasing intensity and during extended durations of higher intensity exercise AMPK activation results are varied with some results supporting and intensity/duration effect and others not. Similarly, CaMKII activation and signaling results following exercise of different intensities and durations are inconsistent. The PGC-1α literature is equally inconsistent with only some studies demonstrating an effect of intensity on post exercise mRNA expression. We present a novel meta-analysis that suggests that the inconsistency in the PGC-1α literature may be due to sample size and statistical power limitations owing to the effect of intensity on PGC-1α expression being small. There is little data available regarding the impact of exercise duration on PGC-1α expression. We highlight the need for future well designed, adequately statistically powered, studies to clarify our understanding of the effects of volume, intensity, and duration on the induction of mitochondrial biogenesis by exercise.

本综述的目的是探索和讨论增加训练量、强度和持续时间对参与线粒体生物发生起始的关键信号蛋白AMPK、CaMKII和PGC-1α磷酸化/激活的影响。具体而言,我们探讨了增强运动方案对AMP/ADP和Ca2+信号传导的影响,以及运动后PGC−1α基因表达的变化。尽管AMP/ADP浓度似乎随着强度的增加和高强度运动的延长持续时间而增加,但AMPK激活结果各不相同,一些结果支持强度/持续时间效应,而另一些结果则不支持。类似地,不同强度和持续时间的运动后CaMKII的激活和信号传导结果是不一致的。PGC-1α文献同样与仅一些研究表明强度对运动后mRNA表达的影响不一致。我们提出了一项新的荟萃分析,表明PGC-1α文献中的不一致性可能是由于样本量和统计能力的限制,因为强度对PGC-1 a表达的影响很小。关于运动时间对PGC-1α表达的影响,目前几乎没有可用的数据。我们强调,未来需要进行精心设计、充分统计的研究,以澄清我们对运动诱导线粒体生物发生的体积、强度和持续时间影响的理解。
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引用次数: 3
Mitochondria: Key modulators of skeletal muscle remodeling 线粒体:骨骼肌重塑的关键调节剂
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2022.10.004
Joe Quadrilatero
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引用次数: 2
Transient changes to metabolic homeostasis initiate mitochondrial adaptation to endurance exercise 代谢稳态的短暂变化启动线粒体对耐力运动的适应
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2022.03.022
Jessica R. Dent , Ben Stocks , Dean G. Campelj , Andrew Philp

Endurance exercise is well established to increase mitochondrial content and function in skeletal muscle, a process termed mitochondrial biogenesis. Current understanding is that exercise initiates skeletal muscle mitochondrial remodeling via modulation of cellular nutrient, energetic and contractile stress pathways. These subtle changes in the cellular milieu are sensed by numerous transduction pathways that serve to initiate and coordinate an increase in mitochondrial gene transcription and translation. The result of these acute signaling events is the promotion of growth and assembly of mitochondria, coupled to a greater capacity for aerobic ATP provision in skeletal muscle. The aim of this review is to highlight the acute metabolic events induced by endurance exercise and the subsequent molecular pathways that sense this transient change in cellular homeostasis to drive mitochondrial adaptation and remodeling.

耐力运动可以增加骨骼肌中的线粒体含量和功能,这一过程被称为线粒体生物发生。目前的理解是,运动通过调节细胞营养、能量和收缩应激途径来启动骨骼肌线粒体重塑。细胞环境中的这些细微变化由许多转导途径感知,这些转导途径用于启动和协调线粒体基因转录和翻译的增加。这些急性信号事件的结果是促进线粒体的生长和组装,再加上骨骼肌中有氧ATP供应的更大能力。这篇综述的目的是强调耐力运动诱导的急性代谢事件,以及随后感知细胞稳态的这种短暂变化以驱动线粒体适应和重塑的分子途径。
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引用次数: 2
Mitochondrial-derived vesicles in skeletal muscle remodeling and adaptation 骨骼肌重构和适应中的线粒体源性囊泡
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2022.03.023
Anna Picca , Flora Guerra , Riccardo Calvani , Roberta Romano , Hélio José Coelho-Junior , Cecilia Bucci , Christiaan Leeuwenburgh , Emanuele Marzetti

Mitochondrial remodeling is crucial to meet the bioenergetic demand to support muscle contractile activity during daily tasks and muscle regeneration following injury. A set of mitochondrial quality control (MQC) processes, including mitochondrial biogenesis, dynamics, and mitophagy, are in place to maintain a well-functioning mitochondrial network and support muscle regeneration. Alterations in any of these pathways compromises mitochondrial quality and may potentially lead to impaired myogenesis, defective muscle regeneration, and ultimately loss of muscle function.

Among MQC processes, mitophagy has gained special attention for its implication in the clearance of dysfunctional mitochondria via crosstalk with the endo-lysosomal system, a major cell degradative route. Along this pathway, additional opportunities for mitochondrial disposal have been identified that may also signal at the systemic level. This communication occurs via inclusion of mitochondrial components within membranous shuttles named mitochondrial-derived vesicles (MDVs).

Here, we discuss MDV generation and release as a mitophagy-complementing route for the maintenance of mitochondrial homeostasis in skeletal myocytes. We also illustrate the possible role of muscle-derived MDVs in immune signaling during muscle remodeling and adaptation.

线粒体重塑对于满足生物能量需求至关重要,以支持日常任务中的肌肉收缩活动和损伤后的肌肉再生。一套线粒体质量控制(MQC)过程,包括线粒体生物发生、动力学和线粒体自噬,已到位,以维持功能良好的线粒体网络并支持肌肉再生。这些途径中的任何一种的改变都会损害线粒体的质量,并可能导致肌肉生成受损、肌肉再生缺陷,最终导致肌肉功能丧失。在MQC过程中,线粒体自噬因其通过与内溶酶体系统(一种主要的细胞降解途径)的相互作用清除功能失调的线粒体而受到特别关注。沿着这一途径,已经确定了线粒体处置的额外机会,这也可能是系统水平的信号。这种通讯是通过将线粒体成分包含在称为线粒体衍生囊泡(MDV)的膜梭中而发生的。在这里,我们讨论了MDV的产生和释放,作为线粒体自噬的补充途径,以维持骨骼肌细胞的线粒体稳态。我们还阐明了肌肉来源的MDV在肌肉重塑和适应过程中的免疫信号传导中的可能作用。
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引用次数: 10
Mitochondrial Apoptotic Signaling Involvement in Remodeling During Myogenesis and Skeletal Muscle Atrophy 线粒体凋亡信号参与肌发生和骨骼肌萎缩过程中的重塑
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2022.01.011
Fasih Ahmad Rahman, Joe Quadrilatero

Mitochondria play a major role in apoptotic signaling. In addition to its role in eliminating dysfunctional cells, mitochondrial apoptotic signaling is implicated as a key component of myogenic differentiation and skeletal muscle atrophy. For example, the activation of cysteine-aspartic proteases (caspases; CASP's) can aid in the initial remodeling stages of myogenic differentiation by cleaving protein kinases, transcription factors, and cytoskeletal proteins. Precise regulation of these signals is needed to prevent excessive cell disassemble and subsequent cell death. During skeletal muscle atrophy, the activation of CASP's and mitochondrial derived nucleases participate in myonuclear fragmentation, a potential loss of myonuclei, and cleavage of contractile structures within skeletal muscle. The B cell leukemia/lymphoma 2 (BCL2) family of proteins play a significant role in regulating myogenesis and skeletal muscle atrophy by governing the initiating steps of mitochondrial apoptotic signaling. This review discusses the role of mitochondrial apoptotic signaling in skeletal muscle remodeling during myogenic differentiation and skeletal muscle pathological states, including aging, disuse, and muscular dystrophy.

线粒体在细胞凋亡信号传导中起着重要作用。除了在消除功能失调细胞方面的作用外,线粒体凋亡信号传导是肌源性分化和骨骼肌萎缩的关键组成部分。例如,半胱氨酸天冬氨酸蛋白酶(caspases;CASP)的激活可以通过裂解蛋白激酶、转录因子和细胞骨架蛋白来帮助肌源性分化的初始重塑阶段。需要精确调节这些信号,以防止过度的细胞分解和随后的细胞死亡。在骨骼肌萎缩期间,CASP和线粒体衍生的核酸酶的激活参与了肌细胞核的断裂、肌细胞核的潜在损失以及骨骼肌内收缩结构的断裂。B细胞白血病/淋巴瘤2(BCL2)蛋白家族通过控制线粒体凋亡信号的起始步骤,在调节肌发生和骨骼肌萎缩中发挥重要作用。这篇综述讨论了线粒体凋亡信号在肌源性分化和骨骼肌病理状态(包括衰老、废用和肌营养不良)过程中骨骼肌重塑中的作用。
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引用次数: 5
Emerging role of mitophagy in myoblast differentiation and skeletal muscle remodeling 线粒体自噬在成肌细胞分化和骨骼肌重塑中的作用。
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2021.11.026
Fasih Ahmad Rahman, Joe Quadrilatero

Mitochondrial turnover in the form of mitophagy is emerging as a central process in maintaining cellular function. The degradation of damaged mitochondria through mitophagy is particularly important in cells/tissues that exhibit high energy demands. Skeletal muscle is one such tissue that requires precise turnover of mitochondria in several conditions in order to optimize energy production and prevent bioenergetic crisis. For instance, the formation of skeletal muscle (i.e., myogenesis) is accompanied by robust turnover of low-functioning mitochondria to eventually allow the formation of high-functioning mitochondria. In mature skeletal muscle, alterations in mitophagy-related signaling occur during exercise, aging, and various disease states. Nonetheless, several questions regarding the direct role of mitophagy in various skeletal muscle conditions remain unknown. Furthermore, given the heterogenous nature of skeletal muscle with respect to various cellular and molecular properties, and the plasticity in these properties in various conditions, the involvement and characterization of mitophagy requires more careful consideration in this tissue. Therefore, this review will highlight the known mechanisms of mitophagy in skeletal muscle, and discuss their involvement during myogenesis and various skeletal muscle conditions. This review also provides important considerations for the accurate measurement of mitophagy and interpretation of data in skeletal muscle.

线粒体以线粒体自噬的形式进行周转是维持细胞功能的核心过程。受损线粒体通过线粒体自噬的降解在表现出高能量需求的细胞/组织中尤为重要。骨骼肌就是这样一种组织,它需要在几种条件下精确地翻转线粒体,以优化能量生产并防止生物能量危机。例如,骨骼肌的形成(即肌生成)伴随着低功能线粒体的强大周转,最终形成高功能线粒体。在成熟的骨骼肌中,线粒体自噬相关信号的改变发生在运动、衰老和各种疾病状态期间。尽管如此,关于线粒体自噬在各种骨骼肌疾病中的直接作用的几个问题仍然未知。此外,考虑到骨骼肌在各种细胞和分子特性方面的异质性,以及这些特性在各种条件下的可塑性,线粒体自噬的参与和表征需要在该组织中进行更仔细的考虑。因此,这篇综述将强调骨骼肌中已知的线粒体自噬机制,并讨论它们在肌发生和各种骨骼肌状况中的作用。这篇综述也为骨骼肌线粒体自噬的准确测量和数据解释提供了重要的考虑因素。
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引用次数: 5
Implications of mitochondrial fusion and fission in skeletal muscle mass and health 线粒体融合和裂变对骨骼肌质量和健康的影响
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2022.02.011
Vanina Romanello , Marco Sandri

The continuous dynamic reshaping of mitochondria by fusion and fission events is critical to keep mitochondrial quality and function under control in response to changes in energy and stress. Maintaining a functional, highly interconnected mitochondrial reticulum ensures rapid energy production and distribution. Moreover, mitochondrial networks act as dynamic signaling hub to adapt to the metabolic demands imposed by contraction, energy expenditure, and general metabolism. However, excessive mitochondrial fusion or fission results in the disruption of the skeletal muscle mitochondrial network integrity and activates a retrograde response from mitochondria to the nucleus, leading to muscle atrophy, weakness and influencing whole-body homeostasis. These actions are mediated via the secretion of mitochondrial-stress myokines such as FGF21 and GDF15. Here we will summarize recent discoveries in the role of mitochondrial fusion and fission in the control of muscle mass and in regulating physiological homeostasis and disease progression.

融合和裂变事件对线粒体的持续动态重塑对于控制线粒体的质量和功能以应对能量和压力的变化至关重要。维持一个功能性的、高度互联的线粒体网确保了能量的快速产生和分配。此外,线粒体网络充当动态信号中枢,以适应收缩、能量消耗和一般代谢带来的代谢需求。然而,过度的线粒体融合或分裂会导致骨骼肌线粒体网络完整性的破坏,并激活从线粒体到细胞核的逆行反应,导致肌肉萎缩、虚弱并影响全身稳态。这些作用是通过线粒体应激性肌细胞因子如FGF21和GDF15的分泌介导的。在这里,我们将总结线粒体融合和分裂在控制肌肉质量、调节生理稳态和疾病进展中的作用的最新发现。
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引用次数: 10
Mitochondrial protein import and UPRmt in skeletal muscle remodeling and adaptation 骨骼肌重塑和适应中的线粒体蛋白输入和UPRmt
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-15 DOI: 10.1016/j.semcdb.2022.01.002
Brandon J. Richards, Mikhaela Slavin, Ashley N. Oliveira, Victoria C. Sanfrancesco, David A. Hood

The biogenesis of mitochondria requires the coordinated expression of the nuclear and the mitochondrial genomes. However, the vast majority of gene products within the organelle are encoded in the nucleus, synthesized in the cytosol, and imported into mitochondria via the protein import machinery, which permit the entry of proteins to expand the mitochondrial network. Once inside, proteins undergo a maturation and folding process brought about by enzymes comprising the unfolded protein response (UPRmt). Protein import and UPRmt activity must be synchronized and matched with mtDNA-encoded subunit synthesis for proper assembly of electron transport chain complexes to avoid proteotoxicity. This review discusses the functions of the import and UPRmt systems in mammalian skeletal muscle, as well as how exercise alters the equilibrium of these pathways in a time-dependent manner, leading to a new steady state of mitochondrial content resulting in enhanced oxidative capacity and improved muscle health.

线粒体的生物发生需要细胞核和线粒体基因组的协调表达。然而,细胞器内的绝大多数基因产物在细胞核中编码,在胞质溶胶中合成,并通过蛋白质输入机制输入线粒体,这允许蛋白质进入以扩大线粒体网络。蛋白质一旦进入体内,就会经历由包括未折叠蛋白质反应(UPRmt)的酶引起的成熟和折叠过程。蛋白质输入和UPRmt活性必须与mtDNA编码的亚基合成同步并匹配,以正确组装电子传输链复合物,避免蛋白毒性。这篇综述讨论了哺乳动物骨骼肌中导入和UPRmt系统的功能,以及运动如何以时间依赖的方式改变这些途径的平衡,导致线粒体含量的新稳定状态,从而增强氧化能力和改善肌肉健康。
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引用次数: 3
Maintenance of neuronal identity in C. elegans and beyond: Lessons from transcription and chromatin factors 秀丽隐杆线虫及其后神经元身份的维持:转录和染色质因子的经验教训。
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-11 DOI: 10.1016/j.semcdb.2023.07.001
Honorine Destain , Manasa Prahlad , Paschalis Kratsios

Neurons are remarkably long-lived, non-dividing cells that must maintain their functional features (e.g., electrical properties, chemical signaling) for extended periods of time – decades in humans. How neurons accomplish this incredible feat is poorly understood. Here, we review recent advances, primarily in the nematode C. elegans, that have enhanced our understanding of the molecular mechanisms that enable post-mitotic neurons to maintain their functionality across different life stages. We begin with “terminal selectors” - transcription factors necessary for the establishment and maintenance of neuronal identity. We highlight new findings on five terminal selectors (CHE-1 [Glass], UNC-3 [Collier/Ebf1–4], LIN-39 [Scr/Dfd/Hox4–5], UNC-86 [Acj6/Brn3a-c], AST-1 [Etv1/ER81]) from different transcription factor families (ZNF, COE, HOX, POU, ETS). We compare the functions of these factors in specific neuron types of C. elegans with the actions of their orthologs in other invertebrate (D. melanogaster) and vertebrate (M. musculus) systems, highlighting remarkable functional conservation. Finally, we reflect on recent findings implicating chromatin-modifying proteins, such as histone methyltransferases and Polycomb proteins, in the control of neuronal terminal identity. Altogether, these new studies on transcription factors and chromatin modifiers not only shed light on the fundamental problem of neuronal identity maintenance, but also outline mechanistic principles of gene regulation that may operate in other long-lived, post-mitotic cell types.

神经元是非常长寿的、不分裂的细胞,必须在很长一段时间内保持其功能特征(如电特性、化学信号)——在人类中是几十年。神经元是如何完成这一令人难以置信的壮举的,人们对此知之甚少。在这里,我们回顾了最新进展,主要是在秀丽隐杆线虫方面,这些进展增强了我们对有丝分裂后神经元在不同生命阶段保持功能的分子机制的理解。我们从“末端选择因子”开始——建立和维持神经元身份所必需的转录因子。我们强调了来自不同转录因子家族(ZNF、COE、HOX、POU、ETS)的五个末端选择子(CHE-1[玻璃]、UNC-3[科利尔/Ebf1-4]、LIN-39[Scr/Dfd/Hox4-5]、UNC-86[Acj6/Brn3a-c]、AST-1[Etv1/ER81])的新发现。我们将这些因子在秀丽隐杆线虫特定神经元类型中的功能与其直系同源物在其他无脊椎动物(黑腹果蝇)和脊椎动物(肌肉线虫)系统中的作用进行了比较,强调了显著的功能保守性。最后,我们回顾了染色质修饰蛋白(如组蛋白甲基转移酶和多梳蛋白)在神经元末端身份控制中的最新发现。总之,这些关于转录因子和染色质修饰物的新研究不仅揭示了神经元身份维持的基本问题,而且概述了可能在其他长寿、有丝分裂后细胞类型中发挥作用的基因调控的机制原理。
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引用次数: 1
Shedding light on mitochondrial outer-membrane permeabilization and membrane potential: State of the art methods and biosensors 揭示线粒体外膜通透性和膜电位:最新的方法和生物传感器
IF 7.3 2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-07-10 DOI: 10.1016/j.semcdb.2023.07.003
Nikolay Popgeorgiev , Clara Gil , Kevin Berthenet , Giulia Bertolin , Gabriel Ichim

Membrane structural integrity is essential for optimal mitochondrial function. These organelles produce the energy needed for all vital processes, provided their outer and inner membranes are intact. This prevents the release of mitochondrial apoptogenic factors into the cytosol and ensures intact mitochondrial membrane potential (ΔΨm) to sustain ATP production. Cell death by apoptosis is generally triggered by outer mitochondrial membrane permeabilization (MOMP), tightly coupled with loss of ΔΨ m. As these two processes are essential for both mitochondrial function and cell death, researchers have devised various techniques to assess them. Here, we discuss current methods and biosensors available for detecting MOMP and measuring ΔΨ m, focusing on their advantages and limitations and discuss what new imaging tools are needed to improve our knowledge of mitochondrial function.

膜结构完整性对于优化线粒体功能至关重要。这些细胞器产生所有生命过程所需的能量,只要它们的内外膜完好无损。这可以防止线粒体凋亡因子释放到细胞质中,并确保完整的线粒体膜电位(ΔΨm)来维持ATP的产生。细胞凋亡通常由外线粒体膜透性(MOMP)触发,并与ΔΨ m的丢失紧密结合。由于这两个过程对线粒体功能和细胞死亡都至关重要,研究人员设计了各种技术来评估它们。在这里,我们讨论了目前用于检测MOMP和测量ΔΨ m的方法和生物传感器,重点讨论了它们的优点和局限性,并讨论了需要哪些新的成像工具来提高我们对线粒体功能的了解。
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引用次数: 4
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