Insulin-Like Growth Factor I Prevents Cellular Aging via Activation of Mitophagy

Hou, Xuwei; Li, Zhaohui; Higashi, Yusuke; Delafontaine, Patrice; Sukhanov, Sergiy

doi:10.1155/2020/4939310

Cited by 19 publications

(20 citation statements)

References 52 publications

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“…In particular, IGF-1 mediates a protective mitochondrial signal that is transduced into the cell through the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). By coupling mitochondrial biogenesis with the induction of BNIP3 (a member of the apoptotic Bcl-2 protein family), this pathway increases autophagosome turnover and improves cell survival, even in the presence of metabolic or mitochondrial stress [84]. In recent years, IGF-1 signaling has been shown to modify mitochondrial function and capacity (including mitochondrial DNA/RNA ratio management), organelle biogenesis, oxidative phosphorylation and suppression of ROS production [85].…”

Section: Igf-1mentioning

confidence: 99%

Biological Aspects of Selected Myokines in Skeletal Muscle: Focus on Aging

Mancinelli

Checcaglini

Coscia

et al. 2021

IJMS

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In the last decade, clear evidence has emerged that the cellular components of skeletal muscle are important sites for the release of proteins and peptides called “myokines”, suggesting that skeletal muscle plays the role of a secretory organ. After their secretion by muscles, these factors serve many biological functions, including the exertion of complex autocrine, paracrine and/or endocrine effects. In sum, myokines affect complex multi-organ processes, such as skeletal muscle trophism, metabolism, angiogenesis and immunological response to different physiological (physical activity, aging, etc.) or pathological states (cachexia, dysmetabolic conditions, chronic inflammation, etc.). The aim of this review is to describe in detail a number of myokines that are, to varying degrees, involved in skeletal muscle aging processes and belong to the group of proteins present in the functional environment surrounding the muscle cell known as the “Niche”. The particular myokines described are those that, acting both from within the cell and in an autocrine manner, have a defined relationship with the modulation of oxidative stress in muscle cells (mature or stem) involved in the regulatory (metabolic or regenerative) processes of muscle aging. Myostatin, IGF-1, NGF, S100 and irisin are examples of specific myokines that have peculiar features in their mechanisms of action. In particular, the potential role of one of the most recently characterized myokines—irisin, directly linked to an active lifestyle—in reducing if not reversing senescence-induced oxidative damage is discussed in terms of its possible application as an agent able to counteract the deleterious effects of muscle aging.

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Section: Igf-1mentioning

confidence: 99%

Biological Aspects of Selected Myokines in Skeletal Muscle: Focus on Aging

Mancinelli

Checcaglini

Coscia

et al. 2021

IJMS

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“…PINK1 is a prime mitophagy regulator.The silencing of PINK1 suppressed mitophagy and inhibited IGF-1-induced anti-ageing impacts in aged SMC, as expected with the pertinent function of mitophagy on the impact ofIGF-1 in cellular ageing. IGF-1 inhibited cellular ageing viaNrf2/ Sirt3-dependent mitophagy activation[20]. Thus, the findings suggest that IGF-1 signaling activation is a viable potential approach for mitophagy activation and retardation of cellular ageing.…”

mentioning

confidence: 80%

“…An antiageing effect was suggested on detection that IGF-1 diminished cell senescence, inhibited DNA telomere shortening, augmented mitochondrial membrane potential, activated cytochrome C oxidase, and minimized mitochondrial DNA derangement in sustained cultured (aged) aortic SMC. IGF-1 enhanced mitophagy in aged cells, and it was associated with mitigated expression of cyclin-dependent kinase inhibitors p16 and p21 and augmented levels of Nrf2 and Sirt3[20], biogenesis in regulators of mitophagy and mitochondria. SiRNAinduced suppression of either Nrf2 or Sirt3 obliterated IGF-1-induced upregulation of mitophagy.…”

mentioning

confidence: 95%

Ageing Influences Mechanisms Which Perturb Insulin Function with Increased Risk in Morbidity and Mortality

Chukwuma¹

2022

MJDO

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Certain modifications or alterations concomitant with ageing include diminished glucose tolerance due to increased insulin resistance from receptor and/or post-receptor perturbations and decrement in pancreatic islet B-cell sensitivity to glucose. Insulin has effects on ageing and lifespan, and provides a mechanism for gene manipulations for people to have prolonged and healthier lives, and as preserved insulin sensitivity is associated with longevity. The insulin function is dependent on mechanisms which are determinants of its circulating abundance, secretion, clearance and sensitivity in its target tissues. Ageing enhances deranging impacts on these processes which debilitate insulin functionality, resulting in augmented risk for morbidity, untoward sequelae and mortality. Certain models of impaired insulin signaling are associated with prolonged longevity or resistance to lifethreatening factors, such as oxidative stress. Insulin and insulin signaling is associated with successful ageing and longevity. This entry enunciates the importance of insulin sensitivity versus secretibility as being critical to the clinical strategy in the treatment, lifestyle changes, early interventions and control of type 2 diabetes. Calorie restriction enhances lifespan in numerous species. Diet manipulation that affects the glucoseinsulin system ostensibly benefits lifespan and diminishes the incidence of ageing-related chronic diseases. During ageing, augmented circulating abundance of glucose and other reducing sugars secondary to agetriggered insulin resistance nonenzymatically reacts with proteins and nucleic acids to debilitate tissue elasticity. Adequate control of factors associated with risks for obesity, diabetes, cardiovascular disease, and other insulin and ageing sequelae can be retarded in the elderly with optimum sustenance of their lifestyles.

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“…The maintenance of smooth muscle cells is potentiated by insulin-like growth factor 1, IGF-1. However, its potential impact on cellular aging [50] or senescence remains unelucidated. IGF-1 was found to diminish cell aging, disrupt DNA telomere dissipation, elevate mitochondrial membrane capacity and capability and cytochrome coxidase activation as well as mitigation of mitochondrial DNA injury in aged or derelict cultured aortic smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

“…It was suggested that the Nrf2/Sirt3 pathway was pertinent for the impact of IGF-1 on mitophagy. A perspicuous regulator of mitophagy is PINK1 that obliterates suppressed mitophagy and inhibited IGF-1-induced anti-aging influences in decrepit smooth muscle cells as characteristic of mitophagy in the impact of IGF-1 in cellular senescence [50]. It is perspicuous that IGF-1 constrains cellular senescence or aging through Nrf2/Sirt3-dependent mitophagy activation.…”

Section: Discussionmentioning

confidence: 99%

Aging, Cellular Senescence and Diabetes Mellitus: Clinicopathological Correlates, Trends and Targets

2020

AHS

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Diabetes and aging correlate with identical organ and system perturbations which are enhanced by concomitant molecular processes such as cellular senescence. Age represents a major risk factor for type 2 diabetes mellitus. It is unclear how senescence contributes to diabetes pathogenesis. Thus, available treatment modalities have not targeted the vital area of the disease. Reversal of untoward features of cellular aging represents a formidable trajectory for novel type 2 diabetes therapies where dissipation of pancreatic beta cells are impaired for insulin secretion. Furthermore, appropriate therapeutic modalities require characterization of defined senescent beta cell populations and the spatiotemporal variations of the expression of senescence genes. Aging is a dynamic public health dilemma in the prevailing demographic transitions in which a vast majority of those from the sixth decade of life increase exponentially in populations. Researchers have attempted to explicate senescence mechanisms via the identification of novel factors which interact with aging and age-related disorders in furtherance of treatment management, quality of life and lifespan regarding diabetes and its complications. An elucidation of the fundamental mechanisms which result in aging and research-oriented focus on healthy aging will mitigate numerous socioeconomic and healthcare encumbrance now and in the future for diabetes mellitus and related conditions.

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Insulin-Like Growth Factor I Prevents Cellular Aging via Activation of Mitophagy

Cited by 19 publications

References 52 publications

Biological Aspects of Selected Myokines in Skeletal Muscle: Focus on Aging

Biological Aspects of Selected Myokines in Skeletal Muscle: Focus on Aging

Ageing Influences Mechanisms Which Perturb Insulin Function with Increased Risk in Morbidity and Mortality

Aging, Cellular Senescence and Diabetes Mellitus: Clinicopathological Correlates, Trends and Targets

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