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  1. Article: Preface - Animal models for aging.

    Houtkooper, Riekelt H

    Biochimica et biophysica acta. Molecular basis of disease

    2018  Volume 1864, Issue 9 Pt A, Page(s) 2679

    MeSH term(s) Aging/genetics ; Aging/physiology ; Animals ; Humans ; Metabolic Diseases ; Models, Animal ; Research
    Language English
    Publishing date 2018-06-22
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0925-4439 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0925-4439 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 1874-9399
    DOI 10.1016/j.bbadis.2018.06.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: NAD<sup>+</sup> to assess health in aging humans.

    Janssens, Georges E / Houtkooper, Riekelt H / Hoeks, Joris

    Aging

    2022  Volume 14, Issue 15, Page(s) 5962–5963

    MeSH term(s) Aging ; Health Status ; Humans ; NAD
    Chemical Substances NAD (0U46U6E8UK)
    Language English
    Publishing date 2022-08-06
    Publishing country United States
    Document type Editorial
    ISSN 1945-4589
    ISSN (online) 1945-4589
    DOI 10.18632/aging.204220
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Identification of longevity compounds with minimized probabilities of side effects.

    Janssens, Georges E / Houtkooper, Riekelt H

    Biogerontology

    2020  Volume 21, Issue 6, Page(s) 709–719

    Abstract: It is hypothesized that treating the general aging population with compounds that slow aging, geroprotectors, could provide many benefits to society, including a reduction of age-related diseases. It is intuitive that such compounds should cause minimal ... ...

    Abstract It is hypothesized that treating the general aging population with compounds that slow aging, geroprotectors, could provide many benefits to society, including a reduction of age-related diseases. It is intuitive that such compounds should cause minimal side effects, since they would be distributed to otherwise healthy individuals for extended periods of time. The question therefore emerges of how we should prioritize geroprotectors discovered in model organisms for clinical testing in humans. In other words, which compounds are least likely to cause harm, while still potentially providing benefit? To systematically answer this question we queried the DrugAge database-containing hundreds of known geroprotectors-and cross-referenced this with a recently published repository of compound side effect predictions. In total, 124 geroprotectors were associated to 800 unique side effects. Geroprotectors with high risks of side effects, some even with risk for death, included lamotrigine and minocycline, while compounds with low side effect risks included spermidine and D-glucosamine. Despite their popularity as top geroprotector candidates for humans, sirolimus and metformin harbored greater risks of side effects than many other candidate geroprotectors, sirolimus being the more severe of the two. Furthermore, we found that a correlation existed between maximum lifespan extension in worms and the likelihood of causing a side effect, suggesting that extreme lifespan extension in model organisms should not necessarily be the priority when screening for novel geroprotectors. We discuss the implications of our findings for prioritizing geroprotectors, suggesting spermidine and D-glucosamine for clinical trials in humans.
    MeSH term(s) Aging/drug effects ; Animals ; Databases, Factual ; Drug-Related Side Effects and Adverse Reactions ; Glucosamine/pharmacology ; Humans ; Longevity/drug effects ; Metformin ; Mice ; Probability ; Spermidine/pharmacology
    Chemical Substances Metformin (9100L32L2N) ; Glucosamine (N08U5BOQ1K) ; Spermidine (U87FK77H25)
    Language English
    Publishing date 2020-06-19
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2047160-9
    ISSN 1573-6768 ; 1389-5729
    ISSN (online) 1573-6768
    ISSN 1389-5729
    DOI 10.1007/s10522-020-09887-7
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  4. Article ; Online: Ophthalmic acid is a glutathione regulating tripeptide.

    Schomakers, Bauke V / Jillings, Sonia L / van Weeghel, Michel / Vaz, Frédéric M / Salomons, Gajja S / Janssens, Georges E / Houtkooper, Riekelt H

    The FEBS journal

    2024  

    Abstract: Since its discovery in 1958 in the lens of cows, ophthalmic acid (OPH) has stood in the shadow of its anti-oxidant analog: glutathione (GSH). Lacking the thiol group that gives GSH many of its important properties, ophthalmic acid's function has remained ...

    Abstract Since its discovery in 1958 in the lens of cows, ophthalmic acid (OPH) has stood in the shadow of its anti-oxidant analog: glutathione (GSH). Lacking the thiol group that gives GSH many of its important properties, ophthalmic acid's function has remained elusive, and it has been widely presumed to be an accidental product of the same enzymes. In this review, we compile evidence demonstrating that OPH is a ubiquitous metabolite found in bacteria, plants, fungi, and animals, produced through several layers of metabolic regulation. We discuss the limitations of the oft-repeated suggestions that aberrations in OPH levels should solely indicate GSH deficiency or oxidative stress. Finally, we discuss the available literature and suggest OPH's role in metabolism as a GSH-regulating tripeptide; controlling both cellular and organelle influx and efflux of GSH, as well as modulating GSH-dependent reactions and signaling. Ultimately, we hope that this review reinvigorates and directs more research into this versatile metabolite.
    Language English
    Publishing date 2024-01-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.17061
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  5. Article: Long noncoding RNAs in cardiometabolic disorders

    Juni, Rio P. / 't Hart, Kelly C. / Houtkooper, Riekelt H. / Boon, Reinier A.

    FEBS letters. 2022 June, v. 596, no. 11

    2022  

    Abstract: The advancement of medical technology has led not only to an increase in life expectancy but also to a rise in aging‐related diseases. Aging promotes metabolic disorders, in turn affecting cardiovascular health. Derailment of biological processes in the ... ...

    Abstract The advancement of medical technology has led not only to an increase in life expectancy but also to a rise in aging‐related diseases. Aging promotes metabolic disorders, in turn affecting cardiovascular health. Derailment of biological processes in the pancreas, liver, adipose tissue, and skeletal muscle impairs glucose and lipid metabolism, and mitochondrial function, triggering the development of diabetes and lipid‐related disorders that inflict damage on cardiac and vascular tissues. Long noncoding RNAs (lncRNAs) regulate a wide range of biological process and are one of the key factors controlling metabolism and mitochondria. Here, we discuss the versatile function of lncRNAs involved in the metabolic regulation of glucose and lipid, and mitochondrial function, and how the dysregulation of lncRNAs induces the development of various metabolic disorders and their cardiovascular consequences.
    Keywords adipose tissue ; diabetes ; glucose ; lipid metabolism ; lipids ; liver ; longevity ; mitochondria ; pancreas ; skeletal muscle
    Language English
    Dates of publication 2022-06
    Size p. 1367-1387.
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note REVIEW
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1002/1873-3468.14370
    Database NAL-Catalogue (AGRICOLA)

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  6. Article ; Online: Confounding factors from inducible systems for spatiotemporal gene expression regulation.

    Wüst, Rob C I / Houtkooper, Riekelt H / Auwerx, Johan

    The Journal of cell biology

    2020  Volume 219, Issue 7

    Abstract: Spatiotemporally regulated targeted gene manipulation is a common way to study the effect of gene variants on phenotypic traits, but the Cre/loxP and Tet-On/Tet-Off systems can affect whole-organism physiology and function due to off-target effects. We ... ...

    Abstract Spatiotemporally regulated targeted gene manipulation is a common way to study the effect of gene variants on phenotypic traits, but the Cre/loxP and Tet-On/Tet-Off systems can affect whole-organism physiology and function due to off-target effects. We highlight some of these adverse effects, including whole-body endocrinology and disturbances in the gut microbiome and in mitochondrial and metabolic function.
    MeSH term(s) Animals ; Artifacts ; CRISPR-Cas Systems ; Doxycycline/adverse effects ; Gene Editing/methods ; Gene Expression Regulation ; Genome ; Integrases/genetics ; Integrases/metabolism ; Mice ; Mice, Transgenic ; Mitochondria/drug effects ; Mitochondria/metabolism ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Response Elements/drug effects ; Tamoxifen/adverse effects ; Tetracycline/adverse effects ; Transfection/methods
    Chemical Substances Receptors, Estrogen ; Tamoxifen (094ZI81Y45) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-) ; Tetracycline (F8VB5M810T) ; Doxycycline (N12000U13O)
    Language English
    Publishing date 2020-05-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202003031
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  7. Article ; Online: Enzyme engineering to fight mitochondrial diseases.

    Zapata-Pérez, Rubén / Houtkooper, Riekelt H

    Nature metabolism

    2020  Volume 2, Issue 3, Page(s) 215–216

    Language English
    Publishing date 2020-07-21
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-020-0177-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The Role of AMPK Signaling in Brown Adipose Tissue Activation.

    van der Vaart, Jamie I / Boon, Mariëtte R / Houtkooper, Riekelt H

    Cells

    2021  Volume 10, Issue 5

    Abstract: Obesity is becoming a pandemic, and its prevalence is still increasing. Considering that obesity increases the risk of developing cardiometabolic diseases, research efforts are focusing on new ways to combat obesity. Brown adipose tissue (BAT) has ... ...

    Abstract Obesity is becoming a pandemic, and its prevalence is still increasing. Considering that obesity increases the risk of developing cardiometabolic diseases, research efforts are focusing on new ways to combat obesity. Brown adipose tissue (BAT) has emerged as a possible target to achieve this for its functional role in energy expenditure by means of increasing thermogenesis. An important metabolic sensor and regulator of whole-body energy balance is AMP-activated protein kinase (AMPK), and its role in energy metabolism is evident. This review highlights the mechanisms of BAT activation and investigates how AMPK can be used as a target for BAT activation. We review compounds and other factors that are able to activate AMPK and further discuss the therapeutic use of AMPK in BAT activation. Extensive research shows that AMPK can be activated by a number of different kinases, such as LKB1, CaMKK, but also small molecules, hormones, and metabolic stresses. AMPK is able to activate BAT by inducing adipogenesis, maintaining mitochondrial homeostasis and inducing browning in white adipose tissue. We conclude that, despite encouraging results, many uncertainties should be clarified before AMPK can be posed as a target for anti-obesity treatment via BAT activation.
    MeSH term(s) AMP-Activated Protein Kinases/physiology ; Adipose Tissue, Brown/cytology ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, Brown/pathology ; Animals ; Cell Culture Techniques ; Energy Metabolism ; Humans ; Mitochondria/metabolism ; Obesity/metabolism ; Thermogenesis
    Chemical Substances AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2021-05-06
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10051122
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  9. Article ; Online: Stimulating the sir2-spargel axis rescues exercise capacity and mitochondrial respiration in a Drosophila model of Barth syndrome.

    Damschroder, Deena / Zapata-Pérez, Rubén / Richardson, Kristin / Vaz, Frédéric M / Houtkooper, Riekelt H / Wessells, Robert

    Disease models & mechanisms

    2022  Volume 15, Issue 10

    Abstract: Cardiolipin (CL) is a phospholipid required for proper mitochondrial function. Tafazzin remodels CL to create highly unsaturated fatty acid chains. However, when TAFAZZIN is mutated, CL remodeling is impeded, leading to mitochondrial dysfunction and the ... ...

    Abstract Cardiolipin (CL) is a phospholipid required for proper mitochondrial function. Tafazzin remodels CL to create highly unsaturated fatty acid chains. However, when TAFAZZIN is mutated, CL remodeling is impeded, leading to mitochondrial dysfunction and the disease Barth syndrome. Patients with Barth syndrome often have severe exercise intolerance, which negatively impacts their overall quality of life. Boosting NAD+ levels can improve symptoms of other mitochondrial diseases, but its effect in the context of Barth syndrome has not been examined. We demonstrate, for the first time, that nicotinamide riboside can rescue exercise tolerance and mitochondrial respiration in a Drosophila Tafazzin mutant and that the beneficial effects are dependent on sir2 and spargel. Overexpressing spargel increased the total abundance of CL in mutants. In addition, muscles and neurons were identified as key targets for future therapies because sir2 or spargel overexpression in either of these tissues is sufficient to restore the exercise capacity of Drosophila Tafazzin mutants.
    MeSH term(s) Animals ; Barth Syndrome ; Cardiolipins ; Drosophila ; Exercise Tolerance ; Fatty Acids, Unsaturated ; Mitochondria ; NAD ; Phospholipids ; Quality of Life ; Respiration ; Transcription Factors
    Chemical Substances Cardiolipins ; Fatty Acids, Unsaturated ; Phospholipids ; Transcription Factors ; NAD (0U46U6E8UK)
    Language English
    Publishing date 2022-10-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049279
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Long noncoding RNAs in cardiometabolic disorders.

    Juni, Rio P / 't Hart, Kelly C / Houtkooper, Riekelt H / Boon, Reinier A

    FEBS letters

    2022  Volume 596, Issue 11, Page(s) 1367–1387

    Abstract: The advancement of medical technology has led not only to an increase in life expectancy but also to a rise in aging-related diseases. Aging promotes metabolic disorders, in turn affecting cardiovascular health. Derailment of biological processes in the ... ...

    Abstract The advancement of medical technology has led not only to an increase in life expectancy but also to a rise in aging-related diseases. Aging promotes metabolic disorders, in turn affecting cardiovascular health. Derailment of biological processes in the pancreas, liver, adipose tissue, and skeletal muscle impairs glucose and lipid metabolism, and mitochondrial function, triggering the development of diabetes and lipid-related disorders that inflict damage on cardiac and vascular tissues. Long noncoding RNAs (lncRNAs) regulate a wide range of biological process and are one of the key factors controlling metabolism and mitochondria. Here, we discuss the versatile function of lncRNAs involved in the metabolic regulation of glucose and lipid, and mitochondrial function, and how the dysregulation of lncRNAs induces the development of various metabolic disorders and their cardiovascular consequences.
    MeSH term(s) Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Glucose/metabolism ; Humans ; Lipids ; Muscle, Skeletal/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
    Chemical Substances Lipids ; RNA, Long Noncoding ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2022-05-26
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1002/1873-3468.14370
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