Mitochondrial protein import and UPRmt in skeletal muscle remodeling and adaptation

Richards, Brandon J.; Slavin, Mikhaela; Oliveira, Ashley N.; Sanfrancesco, Victoria C.; Hood, David A.

doi:10.1016/j.semcdb.2022.01.002

Cited by 10 publications

(3 citation statements)

References 102 publications

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“…( 59 ) demonstrated that activation of the UPRmt requires the dimethylation of lysine 3 of histone 3 (H3K9) in the presence of met-2 and lin-65 , which leads to a compacted and overall silenced chromatin state, while simultaneously, some chromatin portions remain loose, favoring the binding of UPRmt regulators such as DVE-1. On the other hand, UPRmt activation also requires the conserved demethylases JMJD-3.1 and JMJD-1.2 ( 32 ), which reduce chromatin compaction by removing methylation from H3K9 and H3K27, respectively ( 60 , 61 ). Generally, H3K4me3 is regarded as a transcriptionally positive histone modulation, while H3K27me3 is a transcriptionally inhibitory histone modulation ( 62 ).…”

Section: Discussionmentioning

confidence: 99%

The specific mitochondrial unfolded protein response in fast- and slow-twitch muscles of high-fat diet-induced insulin-resistant rats

Zhang

et al. 2023

Front. Endocrinol.

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IntroductionSkeletal muscle insulin resistance (IR) plays an important role in the pathogenesis of type 2 diabetes mellitus. Skeletal muscle is a heterogeneous tissue composed of different muscle fiber types that contribute distinctly to IR development. Glucose transport shows more protection in slow-twitch muscles than in fast-twitch muscles during IR development, while the mechanisms involved remain unclear. Therefore, we investigated the role of the mitochondrial unfolded protein response (UPRmt) in the distinct resistance of two types of muscle in IR.MethodsMale Wistar rats were divided into high-fat diet (HFD) feeding and control groups. We measured glucose transport, mitochondrial respiration, UPRmt and histone methylation modification of UPRmt-related proteins to examine the UPRmt in the slow fiber-enriched soleus (Sol) and fast fiber-enriched tibialis anterior (TA) under HFD conditions.ResultsOur results indicate that 18 weeks of HFD can cause systemic IR, while the disturbance of Glut4-dependent glucose transport only occurred in fast-twitch muscle. The expression levels of UPRmt markers, including ATF5, HSP60 and ClpP, and the UPRmt-related mitokine MOTS-c were significantly higher in slow-twitch muscle than in fast-twitch muscle under HFD conditions. Mitochondrial respiratory function is maintained only in slow-twitch muscle. Additionally, in the Sol, histone methylation at the ATF5 promoter region was significantly higher than that in the TA after HFD feeding.ConclusionThe expression of proteins involved in glucose transport in slow-twitch muscle remains almost unaltered after HFD intervention, whereas a significant decline of these proteins was observed in fast-twitch muscle. Specific activation of the UPRmt in slow-twitch muscle, accompanied by higher mitochondrial respiratory function and MOTS-c expression, may contribute to the higher resistance to HFD in slow-twitch muscle. Notably, the different histone modifications of UPRmt regulators may underlie the specific activation of the UPRmt in different muscle types. However, future work applying genetic or pharmacological approaches should further uncover the relationship between the UPRmt and insulin resistance.

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Section: Discussionmentioning

confidence: 99%

The specific mitochondrial unfolded protein response in fast- and slow-twitch muscles of high-fat diet-induced insulin-resistant rats

Zhang

et al. 2023

Front. Endocrinol.

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“…Mitochondrial unfolded protein response (UPRmt), as a typical mitochondrial nuclear signal transduction process, promotes the high expression of nuclear-encoded mitochondrial stress proteins by transmitting mitochondrial damage signals to the nucleus ( 93 , 94 ), helping to restore mitochondrial protein balance, thereby protecting electron transport chain complexes to avoid proteotoxicity. The maintenance of mitochondrial protein function, including correct folding, aggregation, and necessary degradation, requires the involvement of proteolytic enzymes and molecular chaperones.…”

Section: Mitochondrial Dysfunction Leads To Ovarian Agingmentioning

confidence: 99%

Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions

Ju,

Zhao,

et al. 2024

Front. Endocrinol.

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Mitochondria plays an essential role in regulating cellular metabolic homeostasis, proliferation/differentiation, and cell death. Mitochondrial dysfunction is implicated in many age-related pathologies. Evidence supports that the dysfunction of mitochondria and the decline of mitochondrial DNA copy number negatively affect ovarian aging. However, the mechanism of ovarian aging is still unclear. Treatment methods, including antioxidant applications, mitochondrial transplantation, emerging biomaterials, and advanced technologies, are being used to improve mitochondrial function and restore oocyte quality. This article reviews key evidence and research updates on mitochondrial damage in the pathogenesis of ovarian aging, emphasizing that mitochondrial damage may accelerate and lead to cellular senescence and ovarian aging, as well as exploring potential methods for using mitochondrial mechanisms to slow down aging and improve oocyte quality.

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“…Utilizing novel mitochondria-to-nuclear communication, the transcription of UPR mt genes, including mitochondrial-specific chaperones and proteases, are increased to restore proteostasis within the organelle [ [29] , [30] , [31] ]. UPR mt activation and the adequate expression of MQC enzymes are a critical adaptive mechanism for the maintenance of organelle quality and homeostasis [ [32] , [33] , [34] ].…”

Section: Introductionmentioning

confidence: 99%

ATF5 is a regulator of exercise-induced mitochondrial quality control in skeletal muscle

Slavin

Kumari

Hood

2022

Molecular Metabolism

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Mitochondrial protein import and UPRmt in skeletal muscle remodeling and adaptation

Cited by 10 publications

References 102 publications

The specific mitochondrial unfolded protein response in fast- and slow-twitch muscles of high-fat diet-induced insulin-resistant rats

The specific mitochondrial unfolded protein response in fast- and slow-twitch muscles of high-fat diet-induced insulin-resistant rats

Mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions

ATF5 is a regulator of exercise-induced mitochondrial quality control in skeletal muscle

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