Low-Intensity Exercise Affects Cardiac Fatty Acid Oxidation by Increasing the Nuclear Content of PPARα, FOXO1, and Lipin1 in Fructose-Fed Rats

Kostić, Milan; Korićanac, Goran; Tepavčević, Snežana; Stanišić, Jelena; Romić, Snježana; Ćulafić, Tijana; Ivković, Tamara; Stojiljković, Mojca

doi:10.1089/met.2022.0078

Cited by 6 publications

(8 citation statements)

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“…Given that mammalian forkhead transcription factors (FoxOs) can have an important relationship to cell death pathways during neurodegenerative disorders [2,5,49,259,260,[299][300][301][302][303][304], they are increasingly being recognized as potential therapeutic targets for MS (Figure 1). In particular, the mammalian FOXO proteins of the O class can lead to neuronal cell death through apoptosis and autophagy activation [5,49,50,68,128,203,250,301,[305][306][307][308][309][310][311][312][313][314][315].…”

Section: Mammalian Forkhead Transcription Factors and Multiple Sclerosismentioning

confidence: 99%

“…Other studies suggest that FoxOs in combination with silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) may lead to immune dysregulation and neuronal inflammation during MS [377] (Figure 1). SIRT1 is a member of the sirtuin family (sirtuin 1) and is a histone deacetylase [2,5,98,106,195,299,308,[378][379][380][381][382]. SIRT1 oversees DNA transcription by transferring acetyl groups from ε-N-acetyl lysine amino acids to the histones of DNA.…”

Section: Mammalian Forkhead Transcription Factors and Multiple Sclerosismentioning

confidence: 99%

“…SIRT1 oversees DNA transcription by transferring acetyl groups from ε-N-acetyl lysine amino acids to the histones of DNA. FoxO proteins are deacetylated by SIRT1 as well as other histone deacetylases [18,299,313,321,[383][384][385]. SIRT1 decreases oxidative stress, offers protection to neurons, and can preserve memory function [5,76,78,98,106,380,386,387].…”

Section: Mammalian Forkhead Transcription Factors and Multiple Sclerosismentioning

confidence: 99%

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Cognitive Impairment in Multiple Sclerosis

Maiese

2023

Bioengineering

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Almost three million individuals suffer from multiple sclerosis (MS) throughout the world, a demyelinating disease in the nervous system with increased prevalence over the last five decades, and is now being recognized as one significant etiology of cognitive loss and dementia. Presently, disease modifying therapies can limit the rate of relapse and potentially reduce brain volume loss in patients with MS, but unfortunately cannot prevent disease progression or the onset of cognitive disability. Innovative strategies are therefore required to address areas of inflammation, immune cell activation, and cell survival that involve novel pathways of programmed cell death, mammalian forkhead transcription factors (FoxOs), the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), and associated pathways with the apolipoprotein E (APOE-ε4) gene and severe acute respiratory syndrome coronavirus (SARS-CoV-2). These pathways are intertwined at multiple levels and can involve metabolic oversight with cellular metabolism dependent upon nicotinamide adenine dinucleotide (NAD+). Insight into the mechanisms of these pathways can provide new avenues of discovery for the therapeutic treatment of dementia and loss in cognition that occurs during MS.

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Section: Mammalian Forkhead Transcription Factors and Multiple Sclerosismentioning

confidence: 99%

Section: Mammalian Forkhead Transcription Factors and Multiple Sclerosismentioning

confidence: 99%

Section: Mammalian Forkhead Transcription Factors and Multiple Sclerosismentioning

confidence: 99%

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Cognitive Impairment in Multiple Sclerosis

Maiese

2023

Bioengineering

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“…Human LIPIN1 is the ortholog to PAH1 in yeast. It acts as a PA phosphatase and is also one of the critical regulators of cellular lipid metabolism in nuclear membrane biogenesis and various tissues [ 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ]. Polymorphism in LIPIN isoforms may lead to a poor condition.…”

Section: Ctdnep1 In Nuclear Membrane Biogenesismentioning

confidence: 99%

Research Trends in C-Terminal Domain Nuclear Envelope Phosphatase 1

Rallabandi

Choi

Cha

et al. 2023

Life

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C-terminal domain nuclear envelope phosphatase 1 (CTDNEP1, formerly Dullard) is a member of the newly emerging protein phosphatases and has been recognized in neuronal cell tissues in amphibians. It contains the phosphatase domain in the C-terminal, and the sequences are conserved in various taxa of organisms. CTDNEP1 has several roles in novel biological activities such as neural tube development in embryos, nuclear membrane biogenesis, regulation of bone morphogenetic protein signaling, and suppression of aggressive medulloblastoma. The three-dimensional structure of CTDNEP1 and the detailed action mechanisms of CTDNEP1’s functions have yet to be determined for several reasons. Therefore, CTDNEP1 is a protein phosphatase of interest due to recent exciting and essential works. In this short review, we summarize the presented biological roles, possible substrates, interacting proteins, and research prospects of CTDNEP1.

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“…From the years 2013 to 2016, the prevalence of DM has risen from over nine percent (5). DM is a chronic disorder that affects all organs of the body leading to cardiac disease, retinal disease, hepatic injury, cerebral ischemia, limb amputation, and renal failure (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). Almost one half billion individuals have DM and at least half of the four million deaths that occur per year with DM impact individuals less than seventy years of age (1,7,(19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk

Maiese

2023

Front. Immunol.

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Life expectancy is increasing throughout the world and coincides with a rise in non-communicable diseases (NCDs), especially for metabolic disease that includes diabetes mellitus (DM) and neurodegenerative disorders. The debilitating effects of metabolic disorders influence the entire body and significantly affect the nervous system impacting greater than one billion people with disability in the peripheral nervous system as well as with cognitive loss, now the seventh leading cause of death worldwide. Metabolic disorders, such as DM, and neurologic disease remain a significant challenge for the treatment and care of individuals since present therapies may limit symptoms but do not halt overall disease progression. These clinical challenges to address the interplay between metabolic and neurodegenerative disorders warrant innovative strategies that can focus upon the underlying mechanisms of aging-related disorders, oxidative stress, cell senescence, and cell death. Programmed cell death pathways that involve autophagy, apoptosis, ferroptosis, and pyroptosis can play a critical role in metabolic and neurodegenerative disorders and oversee processes that include insulin resistance, β-cell function, mitochondrial integrity, reactive oxygen species release, and inflammatory cell activation. The silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), AMP activated protein kinase (AMPK), and Wnt1 inducible signaling pathway protein 1 (WISP1) are novel targets that can oversee programmed cell death pathways tied to β-nicotinamide adenine dinucleotide (NAD+), nicotinamide, apolipoprotein E (APOE), severe acute respiratory syndrome (SARS-CoV-2) exposure with coronavirus disease 2019 (COVID-19), and trophic factors, such as erythropoietin (EPO). The pathways of programmed cell death, SIRT1, AMPK, and WISP1 offer exciting prospects for maintaining metabolic homeostasis and nervous system function that can be compromised during aging-related disorders and lead to cognitive impairment, but these pathways have dual roles in determining the ultimate fate of cells and organ systems that warrant thoughtful insight into complex autofeedback mechanisms.

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Low-Intensity Exercise Affects Cardiac Fatty Acid Oxidation by Increasing the Nuclear Content of PPARα, FOXO1, and Lipin1 in Fructose-Fed Rats

Cited by 6 publications

References 73 publications

Cognitive Impairment in Multiple Sclerosis

Cognitive Impairment in Multiple Sclerosis

Research Trends in C-Terminal Domain Nuclear Envelope Phosphatase 1

The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk

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