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Nathan Goodyear

Mitochondrial dysfunction in Parkinson's disease. [Biochim Biophys Acta. 2010] - PubMed... - 0 views

www.ncbi.nlm.nih.gov/...19733240

mitochondrial dysfunction Parkinson's Disease

shared by Nathan Goodyear on 16 May 11 - No Cached
  • nhibitor of complex I of the electron transport chain can induce parkinsonism
  • any lines of evidence suggest that mitochondrial dysfunction plays a central role in the pathogenesis of Parkinson's disease (PD)
  • Nathan Goodyear on 16 May 11
     
    Mitochondrial dysfunction in Parkinson's Disease
Nathan Goodyear

Growth Inhibition of Ovarian Tumor-Initiating Cells by Niclosamide | Molecular Cancer T... - 0 views

mct.aacrjournals.org/...1703.long

Niclosamide Tumor-initiation cells TIC ovarian cancer cancer CSC cancer stem cells

shared by Nathan Goodyear on 16 Apr 18 - No Cached
  • Ovarian cancer is the most lethal gynecologic malignancy and the fifth-most cause of overall cancer death of women in developed countries
  • An increasingly accepted cancer stem cell hypothesis regards tumors as caricatures of normal organs, possessing a hierarchy of cell types, at various stages of aberrant differentiation, descended from precursor tumor-initiating cells (TIC) cells that are highly resistant to conventional cytotoxics
  • Significant changes of gene expression in 2,928 genes were identified after niclosamide treatment for different time periods
  • ...14 more annotations...
  • uncoupling of mitochondrial oxidative phosphorylation is believed to be its anti-helminthic mechanism of action
  • we hypothesized that niclosamides antagonistic effects on OTICs could, in part, be due to its disruption of metabolism
  • Our results showed that genes participating in protein complexes of oxidative phosphorylation were downregulated
  • niclosamide treatment resulted in a more than 20% increase in reactive oxygen species (ROS) in cultured OTICs
  • niclosamide, which has proved to be safe and effective for the past 2 decades against numerous parasites, inhibited OTIC growth both in vitro and in vivo
  • niclosamide represses metabolic enzymes responsible for bioenergetics, biosynthesis, and redox regulation specifically in OTICs, presumably leading to mitochondrial intrinsic apoptosis pathways, loss of tumor stemness, and growth inhibition
  • Niclosamide is believed to inhibit mitochondrial oxidative phosphorylation
  • Niclosamide was reported to inactivate NF-κB, causing mitochondrial damage and the generation of ROS, leading to apoptosis of leukemic stem cells
  • niclosamide were identified in a screen for mTOR-signaling inhibitors
  • mTOR was reported to maintain stemness properties of HSCs by inhibiting mitochondrial biogenesis and ROS levels (39), implying that mTOR inhibitors (such as niclosamide) may interfere with mitochondria and various metabolic pathways in TICs via disruption of antioxidant responses
  • We observed Wnt hyperactivity in OTICs, in agreement with previous hypotheses of Wnt inhibitor effectiveness as an ovarian cancer therapy
  • niclosamide has now been independently identified in screens for Wnt inhibitors
  • downregulation of the Wnt/β-catenin target oncogenes survivin and c-Myc
  • ovarian carcinogenesis, the cell-to-cell signaling pathway Notch (8), were also suppressed by niclosamide (data not shown). These results agree with another recent niclosamide study in leukemia (49), and it has been widely hypothesized that disruption of Notch signaling may represent a highly effective therapy for ovarian and other solid tumors, via its essentiality to maintaining TIC stemness
  • Nathan Goodyear on 16 Apr 18
     
    Niclosamide, common anti-parasitic medication, inhibits cellular metabolism and increases ROS; both of which provide powerful anti-proliferative, anti-cancer treatment mechanism in TICs. Powerful target therapy for cancer stem cells. Also shown to inhibit Wnt stimulated oncogenes survivin and c-Myc, disrupts Notch signaling, inactivates NF-kappaBeta, and inhibits mTOR-signaling.  This has been found in in vitro and in vivo studies.
Nathan Goodyear

Parabens in male infertility-Is there a mitochondrial connection? 10.1016/j.reprotox.20... - 0 views

www.sciencedirect.com/...S0890623808002682

male infertility parabens mitochondrial mitochondria xenobiotics environmental toxins

shared by Nathan Goodyear on 02 Feb 12 - No Cached
  • Nathan Goodyear on 02 Feb 12
     
    parabens effect through mitochondrial disruption in testes?
Nathan Goodyear

Loss of mitochondrial bioenergetic capacity underlies the glucose avidity of carcinomas - 0 views

cancerres.aacrjournals.org/...9013.full.pdf

Warburg Warburg effect mitochondria mitochondrial bioenergetic capacity glucose cancer

shared by Nathan Goodyear on 11 Jul 13 - No Cached
  • Nathan Goodyear on 11 Jul 13
     
    Is cancer merely a result of mitochondrial and glucose dysfunction? Is cancer really just a energy problem? Good review of the Warburg effect at the biochemistry level in cancer.
Nathan Goodyear

Uric acid induces hepatic steatosis by generatio... [J Biol Chem. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...23035112

uric acid mitochondria non-alcoholic fatty liver fructose triglyceride oxidative stress fatty liver liver ATP

shared by Nathan Goodyear on 01 Oct 13 - No Cached
  • Nathan Goodyear on 01 Oct 13
     
    Elevated uric acid levels up regulate fructose metabolism to triglycerides and fatty liver.  This study finds that liver mitochondrial oxidative stress is also evident.  This mitochondrial dysfunction also leads to compromised ATP production and fat accumulation specifically through inhibition of aconitase..
Nathan Goodyear

Chronic Testosterone Replacement Exerts Cardioprotection against Cardiac Ischemia-Reper... - 0 views

www.ncbi.nlm.nih.gov/...PMC4379072

cardiovascular disease cardiovascular disease heart health Testosterone low T low Testosterone hormone hormones

shared by Nathan Goodyear on 04 Jun 15 - No Cached
  • In this study, the cardioprotective effects of testosterone in testosterone-deprived rats heart with I/R injury were demonstrated
  • Prior to I/R injury, testosterone replacement provided cardioprotective effects in testosterone-deprived rats as indicated by (1) improved cardiac functions by markedly preserved %EF and %FS, and (2) attenuated cardiac sympathovagal imbalance by a markedly decreased LF/HF ratio
  • Testosterone replacement exerts cardioprotective effects by improving left ventricular function and cardiac sympathovagal balance impaired by testosterone deprivation in ORX rats
  • ...3 more annotations...
  • During the I/R period, testosterone replacement in ORX rats exerted the beneficial effects as indicated by (1) improved left ventricular pressure; (2) markedly decreased infarct size; (3) reduced fatal cardiac arrhythmias by increased time to 1st VT/VF onset and reduced arrhythmia scores; and (4) attenuated cardiac mitochondrial dysfunction caused by I/R injury by reducing ROS production, cardiac mitochondrial swelling and mitochondria membrane depolarization.
  • Chronic testosterone replacement also ameliorates left ventricular dysfunction, and reduces the infarct size and cardiac arrhythmias impaired by I/R injury under testosterone-deprived conditions
  • The mechanisms responsible for these beneficial effects of testosterone could be due to its ability to attenuate cardiac mitochondrial dysfunction and cardiomyocyte apoptosis
  • Nathan Goodyear on 04 Jun 15
     
    animal study finds that Testosterone therapy is cardioprotective in a preventative mode and with myocardial injury.  Normalization of Testosterone in these animals with low T reduced infant injury size and improved heart function.  
Nathan Goodyear

Mitochondrial-nuclear epistasis: Implications for ... [Ageing Res Rev. 2010] - PubMed r... - 0 views

www.ncbi.nlm.nih.gov/...20601194

mitochondrial aging

shared by Nathan Goodyear on 14 Jan 11 - No Cached
  • There is substantial evidence that mitochondria are involved in the aging process
  • Nathan Goodyear on 14 Jan 11
     
    Mitochondrial-nuclear epistasis: Implications for human aging and longevity.
Nathan Goodyear

Mitochondrial DNA mutations as an important contri... [Lancet. 1989] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...2564461

dna mitochondrial mutations

shared by Nathan Goodyear on 14 Jan 11 - No Cached
  • Nathan Goodyear on 14 Jan 11
     
    Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases.
Nathan Goodyear

Brain mitochondrial dysfunction in aging. [IUBMB Life. 2008] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...18421773

mitochondrial brain dysfunction aging

shared by Nathan Goodyear on 08 Feb 11 - No Cached
  • Nathan Goodyear on 08 Feb 11
     
    decreased mitochondrial dysfunction in brain leads to aging and poor function of brain
Nathan Goodyear

Oxidative stress, mitochondrial DNA mutation, and ... [Exp Biol Med (Maywood). 2002] - ... - 0 views

www.ncbi.nlm.nih.gov/...12324649

stress mitochondrial oxidative aging

shared by Nathan Goodyear on 08 Feb 11 - No Cached
  • Nathan Goodyear on 08 Feb 11
     
    oxidative stress, mitochondrial damage, and aging
Nathan Goodyear

Mitochondrial disorders. [Curr Opin Neurol. 2007] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...17885446

mitochondrial neurodegenerative disease

shared by Nathan Goodyear on 07 Feb 11 - No Cached
  • Nathan Goodyear on 07 Feb 11
     
    mitochondrial medicine and contribution to neurodegenerative diseases
Nathan Goodyear

Mitochondrial dysfunction and oxidative damage in ... [J Bioenerg Biomembr. 2004] - Pub... - 0 views

www.ncbi.nlm.nih.gov/...15377876

mitochondrial dysfunction CoQ10 neurodegenerative diseases

shared by Nathan Goodyear on 07 Feb 11 - No Cached
  • he increasing evidence that Parkinson's disease is associated with abnormalities in the electron transport gene as well as oxidative damage
  • Nathan Goodyear on 07 Feb 11
     
    CoQ10 useful to improve mitochondrial function and thus treatment of neurodegenerative diseases
Nathan Goodyear

Oxidative stress, mitochondrial dysfunction and ce... [J Neurol Sci. 2005] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...15896810

CoQ10 mitochondria neurodegenerative disease Alzheimer's Parkinsons MS ALS oxidative stress

shared by Nathan Goodyear on 07 Feb 11 - No Cached
  • There is significant evidence that the pathogenesis of several neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, Friedreich's ataxia (FRDA), multiple sclerosis and amyotrophic lateral sclerosis, may involve the generation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) associated with mitochondrial dysfunction
  • Nathan Goodyear on 07 Feb 11
     
    Mitochondrial dysfunction at heart of diseases such as Parkinson's, Alzheimers, MS, ALS..
Nathan Goodyear

Mitochondrial disorders - 0 views

brain.oxfordjournals.org/...2153.abstract

mitochondrial disorders

shared by Nathan Goodyear on 03 Mar 11 - No Cached
  • Nathan Goodyear on 03 Mar 11
     
    highly technical discussion on mitochondrial disorders
Nathan Goodyear

Mitochondrial dysfunction in distal axons contributes to human immunodeficiency virus s... - 0 views

onlinelibrary.wiley.com/...abstract

mitochondrial dysfunction neuropathy

shared by Nathan Goodyear on 18 May 11 - No Cached
  • Nathan Goodyear on 18 May 11
     
    mitochondrial damage associated with neuropathy
Nathan Goodyear

Mitochondrial dysfunction in Parkinson's disease: ... [Parkinsons Dis. 2010] - PubMed r... - 0 views

www.ncbi.nlm.nih.gov/...21234411

mitochondrial dysfunction Parkinson's disease neurodegenerative

shared by Nathan Goodyear on 16 May 11 - No Cached
  • Nathan Goodyear on 16 May 11
     
    fantastic read on mitochondrial dysfunction and parkinson's disease
Nathan Goodyear

Role of Oxidative Stress and the Microenvironment in Breast Cancer Development and Prog... - 0 views

www.ncbi.nlm.nih.gov/...PMC3950899

cancer oxidative stress warburg effect reverse warburg effect ROS

shared by Nathan Goodyear on 11 Nov 14 - No Cached
  • oxidative stress leads to HIF-1α accumulation
  • increased levels of hydrogen peroxide in exhaled breath condensate from patients with localized breast malignancy, associated with increased clinical severity
  • Oxidative stress generated by breast cancer cells activates HIF-1α and NFκB in fibroblasts, leading to autophagy and lysosomal degradation of Cav-1
  • ...18 more annotations...
  • Comparing mitochondrial metabolic activity revealed a difference between stroma and epithelial cells
  • metalloproteinases (MMP) such as MMP-2, MMP-3, and MMP-9 increase extracellular matrix turnover and are themselves activated by oxidative stress
  • Overexpression of NOX4 in normal breast epithelial cells results in cellular senescence, resistance to apoptosis, and tumorigenic transformation, as well as increased aggressiveness of breast cancer cells
  • Lowered expression of Cav-1 not only leads to myofibroblast conversion and inflammation but also seems to impact aerobic glycolysis, leading to secretion of high energy metabolites such as pyruvate and lactate that drive mitochondrial oxidative phosphorylation in cancer cells
  • Reverse Warburg Effect
  • secreted transforming growth factor β (TGFβ), insulin-like growth factor (IGF), platelet-derived growth factor (PDGF), fibroblast growth factor 2, and stromal-derived factor 1 (SDF1) are able to activate fibroblasts and increase cancer cell proliferation
  • oxidative stress has an important role in the initiation and preservation of breast cancer progression
  • cancer preventive role of healthy mitochondria
  • the cancer cells produce hydrogen peroxide and by driving the “Reverse Warburg Effect” initiate oxidative stress in fibroblasts. As a result of this process, fibroblasts exhibited reduced mitochondrial activity, increased glucose uptake, ROS, and metabolite production.
  • Oxidative stress results from an imbalance between unstable reactive species lacking one or more unpaired electrons (superoxide anion, hydrogen peroxide, hydroxyl radical, reactive nitrogen species) and antioxidants
  • cancer cells are able to induce drivers of oxidative stress, autophagy and mitophagy: HIF-1α and NFκB in surrounding stroma fibro-blasts
  • Studies show that loss of Cav-1 in adjacent breast cancer stroma fibroblasts can be prevented by treatment with N-acetyl cysteine, quercetin, or metformin
  • However, diets rich in antioxidants have fallen short in sufficiently preventing cancer
  • obstructing oxidative stress in the tumor microenvironment can lead to mitophagy and promote breast cancer shutdown is a promising discovery for the development of future therapeutic interventions.
  • It is widely held that HIF-1α function is dependent upon its location within the tumor microenvironment. It acts as a tumor promoter in CAFs and as a tumor suppressor in cancer cells
  • It was reported that overexpression of recombinant (SOD2) (Trimmer et al., 2011) or injection of SOD, catalase, or their pegylated counterparts can block recurrence and metastasis in mice
  • hydrogen peroxide is one of the main factors that can push fibroblasts and cancer cells into senescence
  • Recent studies show that in the breast cancer microenvironment, oxidative stress causes mitochondrial dysfunction
  • Nathan Goodyear on 11 Nov 14
     
    Really fascinating article on tumor signaling. The article points to a complex signaling between cancer cells and stromal fibroblasts that results in myofibroblast transformation that increases the microenvironment favorability of cancer. This article points to oxidative stress as the primary driving force.  
Nathan Goodyear

Estrogenic regulation of skeletal muscle proteome: a study of premenopausal women and p... - 0 views

onlinelibrary.wiley.com/...full

estradiol menopause muscle hormones mitochondria aging female

shared by Nathan Goodyear on 10 Oct 17 - No Cached
  • Female aging is characterized by menopausal change in sex steroid hormones concomitant to increase in aging-related decrements in skeletal muscle performance that can be attenuated by HRT use
  • The major canonical pathways found to be differentially regulated included mitochondrial dysfunction, oxidative phosphorylation, glycolysis, and TCA-cycle, strong indicators for affected energy metabolism
  • E2 to exert anti-apoptotic effects in muscle progenitor cells by improving mitochondrial function
  • ...2 more annotations...
  • E2 is a major regulator of human skeletal muscle signaling in women
  • After menopause, when ovarian E2 production is ceased, the prevalence of cardio-metabolic diseases increases. Our result that different trajectories of the energy pathways in the skeletal muscle may be regulated by E2 provides candidate molecules as key targets for future interventions to prevent or treat postmenopausal metabolic dysregulation
  • Nathan Goodyear on 10 Oct 17
     
    Study finds Estradiol regulates human skeletal muscle cell signaling (mitochondrial function, oxidative phosphorylation, glycolysis, and TCA cycle) in study of pre/post menopause women through proteome analysis. This study would have been complete if they had carried to search beyond that of protein to epigenetics.
Nathan Goodyear

American College of Cardiology Foundation | Journal of the American College of Cardiolo... - 0 views

content.onlinejacc.org/article.aspx

statin therapy statins CoQ10 mitochondria

shared by Nathan Goodyear on 18 Mar 13 - No Cached
  • Nathan Goodyear on 18 Mar 13
     
    Small study, but well designed study shows that statins inhibit CoQ10 mediated oxidative phosphorylation through decrease in CoQ10.  This points directly at a decrease in mitochondrial function as a result of statin therapy.
Nathan Goodyear

ScienceDirect.com - Physiology & Behavior - Mitochondrial complex I inhibition depletes... - 0 views

www.sciencedirect.com/...S0031938404003403

testosterone mitochondria parkinson's disease Parkinson's

shared by Nathan Goodyear on 21 May 13 - No Cached
  • Nathan Goodyear on 21 May 13
     
    Testosterone is known to provide anti-inflammatory signaling in men.  This study, inhibition of mitochondrial complex I (coQ dependent) resulted in lower testosterone in rat models.  One of the major side effects of statin therapy is poor memory and brain fog. Hmmm.
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