Mitochondrial biogenesis: An update

Popov, Lucia-Doina

doi:10.1111/jcmm.15194

Cited by 435 publications

(270 citation statements)

References 87 publications

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“…Furthermore, their regulations on transcription or post-translation level are responsive to meet the multiple metabolic demands induced by physiological signals, senescence, and diseases ( Cui et al, 2006 ; Bellance et al, 2009 ; D’Errico et al, 2011 ; Patel et al, 2012 ; Tsunemi and La Spada, 2012 ). For instance, PGC1-related coactivators can activate the expression of NRF1, NRF2, and transcription factor A (TFAM, the final effectors of mtDNA transcription and replication) to regulate the expression of respiratory chain and the biogenesis of mitochondria, a process that has been well-documented in previous reviews ( Gleyzer et al, 2005 ; Scarpulla, 2008 ; Scarpulla et al, 2012 ; Villena, 2015 ; Popov, 2020 ). Therefore, we commonly regard the expression of PGC1 α, NRF1 , TFAM , and mitochondrial-related genes, as well as mtDNA copy number as the markers for mitochondrial biogenesis.…”

Section: Overview Of the Mitochondrial Biogenesismentioning

confidence: 93%

A Balanced Act: The Effects of GH–GHR–IGF1 Axis on Mitochondrial Function

Zhang

2021

Front. Cell Dev. Biol.

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Mitochondrial function is multifaceted in response to cellular energy homeostasis and metabolism, with the generation of adenosine triphosphate (ATP) through the oxidative phosphorylation (OXPHOS) being one of their main functions. Selective elimination of mitochondria by mitophagy, in conjunction with mitochondrial biogenesis, regulates mitochondrial function that is required to meet metabolic demand or stress response. Growth hormone (GH) binds to the GH receptor (GHR) and induces the JAK2/STAT5 pathway to activate the synthesis of insulin-like growth factor 1 (IGF1). The GH–GHR–IGF1 axis has been recognized to play significant roles in somatic growth, including cell proliferation, differentiation, division, and survival. In this review, we describe recent discoveries providing evidence for the contribution of the GH–GHR–IGF1 axis on mitochondrial biogenesis, mitophagy (or autophagy), and mitochondrial function under multiple physiological conditions. This may further improve our understanding of the effects of the GH–GHR–IGF1 axis on mitochondrial function, which may be controlled by the delicate balance between mitochondrial biogenesis and mitophagy. Specifically, we also highlight the challenges that remain in this field.

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Section: Overview Of the Mitochondrial Biogenesismentioning

confidence: 93%

A Balanced Act: The Effects of GH–GHR–IGF1 Axis on Mitochondrial Function

Zhang

2021

Front. Cell Dev. Biol.

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“…Mitochondrial abundance is regulated by the fine-tuning of new organelle generation by mitochondrial biogenesis and removing dysfunctional organelles by mitophagy. Mitochondrial biogenesis involves the nuclear–mitochondrial coordination of transcription, translation, and import of new proteins into pre-existing organelles [ 31 ]. The coactivators PGC-1α and PGC-1β (peroxisome proliferator-activated receptor-γ coactivator-1α and β), the master regulators of the mitochondriogenesis process, are activated by stimuli that alter the cellular energy demands such as exercise, fasting, and cold exposure [ 32 ].…”

Section: Mitochondrial Plasticity Declines In Aging Sarcopeniamentioning

confidence: 99%

The Interplay between Mitochondrial Morphology and Myomitokines in Aging Sarcopenia

Romanello

2020

IJMS

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Sarcopenia is a chronic disease characterized by the progressive loss of skeletal muscle mass, force, and function during aging. It is an emerging public problem associated with poor quality of life, disability, frailty, and high mortality. A decline in mitochondria quality control pathways constitutes a major mechanism driving aging sarcopenia, causing abnormal organelle accumulation over a lifetime. The resulting mitochondrial dysfunction in sarcopenic muscles feedbacks systemically by releasing the myomitokines fibroblast growth factor 21 (FGF21) and growth and differentiation factor 15 (GDF15), influencing the whole-body homeostasis and dictating healthy or unhealthy aging. This review describes the principal pathways controlling mitochondrial quality, many of which are potential therapeutic targets against muscle aging, and the connection between mitochondrial dysfunction and the myomitokines FGF21 and GDF15 in the pathogenesis of aging sarcopenia.

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“…We employed levels of peroxisome proliferator-activated receptor gamma-coactivator 1-alpha (PGC-1α) and ATP synthase subunit beta (ATPB) as proxies for mitochondrial content and function. PGC-1α is a transcriptional coactivator and central inducer of mitochondrial biogenesis [ 34 ], while ATPB is a member of the complex V of the electron transport chain in the inner membrane of the mitochondria and commonly used as a mitochondrial marker. Interestingly, BAT of female Trsp f/f -Ucp1-Cre +/− mice presented increased levels of both PGC-1α ( Figure 4 a) and ATPB ( Figure 4 b), while male Trsp f/f -Ucp1-Cre +/− mice kept similar expression levels of both markers.…”

Section: Resultsmentioning

confidence: 99%

Adaptive Thermogenesis in a Mouse Model Lacking Selenoprotein Biosynthesis in Brown Adipocytes

Seale

Ogawa-Wong

Watanabe

et al. 2021

IJMS

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Selenoproteins are a class of proteins with the selenium-containing amino acid selenocysteine (Sec) in their primary structure. Sec is incorporated into selenoproteins via recoding of the stop codon UGA, with specific cis and trans factors required during translation to avoid UGA recognition as a stop codon, including a Sec-specific tRNA, tRNA[Ser]Sec, encoded in mice by the gene Trsp. Whole-body deletion of Trsp in mouse is embryonically lethal, while targeted deletion of Trsp in mice has been used to understand the role of selenoproteins in the health and physiology of various tissues. We developed a mouse model with the targeted deletion of Trsp in brown adipocytes (Trspf/f-Ucp1-Cre+/−), a cell type predominant in brown adipose tissue (BAT) controlling energy expenditure via activation of adaptive thermogenesis, mostly using uncoupling protein 1 (Ucp1). At room temperature, Trspf/f-Ucp1-Cre+/− mice maintain oxygen consumption and Ucp1 expression, with male Trspf/f-Ucp1-Cre+/− mice accumulating more triglycerides in BAT than both female Trspf/f-Ucp1-Cre+/− mice or Trspf/f controls. Acute cold exposure neither reduced core body temperature nor changed the expression of selenoprotein iodothyronine deiodinase type II (Dio2), a marker of adaptive thermogenesis, in Trspf/f-Ucp1-Cre+/− mice. Microarray analysis of BAT from Trspf/f-Ucp1-Cre+/− mice revealed glutathione S-transferase alpha 3 (Gsta3) and ELMO domain containing 2 (Elmod2) as the transcripts most affected by the loss of Trsp. Male Trspf/f-Ucp1-Cre+/− mice showed mild hypothyroidism while downregulating thyroid hormone-responsive genes Thrsp and Tshr in their BATs. In summary, modest changes in the BAT of Trspf/f-Ucp1-Cre +/− mice implicate a mild thyroid hormone dysfunction in brown adipocytes.

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Mitochondrial biogenesis: An update

Cited by 435 publications

References 87 publications

A Balanced Act: The Effects of GH–GHR–IGF1 Axis on Mitochondrial Function

A Balanced Act: The Effects of GH–GHR–IGF1 Axis on Mitochondrial Function

The Interplay between Mitochondrial Morphology and Myomitokines in Aging Sarcopenia

Adaptive Thermogenesis in a Mouse Model Lacking Selenoprotein Biosynthesis in Brown Adipocytes

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