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  1. AU="Mezdari, Zaineb"
  2. AU=Wilkinson Beverley
  3. AU=Halbower Ann C AU=Halbower Ann C
  4. AU="Ghosh, Ananya"
  5. AU="Spoletini, Gabriele"
  6. AU="Gracefo, Sara"
  7. AU="Works, Kaitlyn R"
  8. AU="LIU Lei"
  9. AU="McLennan, John D"
  10. AU=Dickinson Gordon M AU=Dickinson Gordon M
  11. AU=Hertzler Dean A 2nd
  12. AU="Yan, Xinrui"
  13. AU="Seal, M L"
  14. AU="Seka, Devin J"
  15. AU="Nguyen, Phuong T B"

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  1. Artikel ; Online: Response by Sawaki et al to Letter Regarding Article, "Visceral Adipose Tissue Drives Cardiac Aging Through Modulation of Fibroblast Senescence by Osteopontin Production".

    Sawaki, Daigo / Czibik, Gabor / Pini, Maria / Mezdari, Zaineb / Zhang, Yanyan / Henegar, Corneliu / Derumeaux, Geneviève

    Circulation

    2019  Band 139, Heft 6, Seite(n) 845–846

    Mesh-Begriff(e) Cellular Senescence ; Fibroblasts ; Heart ; Intra-Abdominal Fat ; Osteopontin
    Chemische Substanzen Osteopontin (106441-73-0)
    Sprache Englisch
    Erscheinungsdatum 2019-02-04
    Erscheinungsland United States
    Dokumenttyp Letter ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.118.038482
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Osteopontin promotes age-related adipose tissue remodeling through senescence-associated macrophage dysfunction.

    Sawaki, Daigo / Zhang, Yanyan / Mohamadi, Amel / Pini, Maria / Mezdari, Zaineb / Lipskaia, Larissa / Naushad, Suzain / Lamendour, Lucille / Altintas, Dogus Murat / Breau, Marielle / Liang, Hao / Halfaoui, Maissa / Delmont, Thaïs / Surenaud, Mathieu / Rousseau, Déborah / Yoshimitsu, Takehiko / Louache, Fawzia / Adnot, Serge / Henegar, Corneliu /
    Gual, Philippe / Czibik, Gabor / Derumeaux, Geneviève

    JCI insight

    2023  Band 8, Heft 8

    Abstract: Adipose tissue macrophages (ATMs) play an important role in obesity and inflammation, and they accumulate in adipose tissue (AT) with aging. Furthermore, increased ATM senescence has been shown in obesity-related AT remodeling and dysfunction. However, ... ...

    Abstract Adipose tissue macrophages (ATMs) play an important role in obesity and inflammation, and they accumulate in adipose tissue (AT) with aging. Furthermore, increased ATM senescence has been shown in obesity-related AT remodeling and dysfunction. However, ATM senescence and its role are unclear in age-related AT dysfunction. Here, we show that ATMs (a) acquire a senescence-like phenotype during chronological aging; (b) display a global decline of basic macrophage functions such as efferocytosis, an essential process to preserve AT homeostasis by clearing dysfunctional or apoptotic cells; and (c) promote AT remodeling and dysfunction. Importantly, we uncover a major role for the age-associated accumulation of osteopontin (OPN) in these processes in visceral AT. Consistently, loss or pharmacologic inhibition of OPN and bone marrow transplantation of OPN-/- mice attenuate the ATM senescence-like phenotype, preserve efferocytosis, and finally restore healthy AT homeostasis in the context of aging. Collectively, our findings implicate pharmacologic OPN inhibition as a viable treatment modality to counter ATM senescence-mediated AT remodeling and dysfunction during aging.
    Mesh-Begriff(e) Mice ; Animals ; Osteopontin/genetics ; Obesity/genetics ; Adipose Tissue ; Macrophages ; Phagocytosis
    Chemische Substanzen Osteopontin (106441-73-0)
    Sprache Englisch
    Erscheinungsdatum 2023-04-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.145811
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Adipose tissue senescence is mediated by increased ATP content after a short-term high-fat diet exposure.

    Pini, Maria / Czibik, Gabor / Sawaki, Daigo / Mezdari, Zaineb / Braud, Laura / Delmont, Thaïs / Mercedes, Raquel / Martel, Cécile / Buron, Nelly / Marcelin, Geneviève / Borgne-Sanchez, Annie / Foresti, Roberta / Motterlini, Roberto / Henegar, Corneliu / Derumeaux, Geneviève

    Aging cell

    2021  Band 20, Heft 8, Seite(n) e13421

    Abstract: In the context of obesity, senescent cells accumulate in white adipose tissue (WAT). The cellular underpinnings of WAT senescence leading to insulin resistance are not fully elucidated. The objective of the current study was to evaluate the presence of ... ...

    Abstract In the context of obesity, senescent cells accumulate in white adipose tissue (WAT). The cellular underpinnings of WAT senescence leading to insulin resistance are not fully elucidated. The objective of the current study was to evaluate the presence of WAT senescence early after initiation of high-fat diet (HFD, 1-10 weeks) in 5-month-old male C57BL/6J mice and the potential role of energy metabolism. We first showed that WAT senescence occurred 2 weeks after HFD as evidenced in whole WAT by increased senescence-associated ß-galactosidase activity and cyclin-dependent kinase inhibitor 1A and 2A expression. WAT senescence affected various WAT cell populations, including preadipocytes, adipose tissue progenitors, and immune cells, together with adipocytes. WAT senescence was associated with higher glycolytic and mitochondrial activity leading to enhanced ATP content in HFD-derived preadipocytes, as compared with chow diet-derived preadipocytes. One-month daily exercise, introduced 5 weeks after HFD, was an effective senostatic strategy, since it reversed WAT cellular senescence, while reducing glycolysis and production of ATP. Interestingly, the beneficial effect of exercise was independent of body weight and fat mass loss. We demonstrated that WAT cellular senescence is one of the earliest events occurring after HFD initiation and is intimately linked to the metabolic state of the cells. Our data uncover a critical role for HFD-induced elevated ATP as a local danger signal inducing WAT senescence. Exercise exerts beneficial effects on adipose tissue bioenergetics in obesity, reversing cellular senescence, and metabolic abnormalities.
    Mesh-Begriff(e) Adenosine Triphosphate/metabolism ; Adipose Tissue/physiopathology ; Animals ; Diet, High-Fat/adverse effects ; Energy Metabolism/physiology ; Male ; Mice
    Chemische Substanzen Adenosine Triphosphate (8L70Q75FXE)
    Sprache Englisch
    Erscheinungsdatum 2021-07-18
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.13421
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Dysregulated Phenylalanine Catabolism Plays a Key Role in the Trajectory of Cardiac Aging.

    Czibik, Gabor / Mezdari, Zaineb / Murat Altintas, Dogus / Bréhat, Juliette / Pini, Maria / d'Humières, Thomas / Delmont, Thaïs / Radu, Costin / Breau, Marielle / Liang, Hao / Martel, Cecile / Abatan, Azania / Sarwar, Rizwan / Marion, Ophélie / Naushad, Suzain / Zhang, Yanyan / Halfaoui, Maissa / Suffee, Nadine / Morin, Didier /
    Adnot, Serge / Hatem, Stéphane / Yavari, Arash / Sawaki, Daigo / Derumeaux, Geneviève

    Circulation

    2021  Band 144, Heft 7, Seite(n) 559–574

    Abstract: Background: Aging myocardium undergoes progressive cardiac hypertrophy and interstitial fibrosis with diastolic and systolic dysfunction. Recent metabolomics studies shed light on amino acids in aging. The present study aimed to dissect how aging leads ... ...

    Abstract Background: Aging myocardium undergoes progressive cardiac hypertrophy and interstitial fibrosis with diastolic and systolic dysfunction. Recent metabolomics studies shed light on amino acids in aging. The present study aimed to dissect how aging leads to elevated plasma levels of the essential amino acid phenylalanine and how it may promote age-related cardiac dysfunction.
    Methods: We studied cardiac structure and function, together with phenylalanine catabolism in wild-type (WT) and p21
    Results: Natural aging is associated with a progressive increase in plasma phenylalanine levels concomitant with cardiac dysfunction, whereas p21 deletion delayed these changes. Phenylalanine treatment induced premature cardiac deterioration in young WT mice, strikingly akin to that occurring with aging, while triggering cellular senescence, redox, and epigenetic changes. Pharmacological restoration of phenylalanine catabolism with tetrahydrobiopterin administration or dietary phenylalanine restriction abrogated the rise in plasma phenylalanine and reversed cardiac senescent alterations in aged WT mice. Observations from aged mice and human samples implicated age-related decline in hepatic phenylalanine catabolism as a key driver of elevated plasma phenylalanine levels and showed increased myocardial PAH-mediated phenylalanine catabolism, a novel signature of cardiac aging.
    Conclusions: Our findings establish a pathogenic role for increased phenylalanine levels in cardiac aging, linking plasma phenylalanine levels to cardiac senescence via dysregulated phenylalanine catabolism along a hepatic-cardiac axis. They highlight phenylalanine/PAH modulation as a potential therapeutic strategy for age-associated cardiac impairment.
    Mesh-Begriff(e) Aging/metabolism ; Aging/pathology ; Amino Acids/metabolism ; Animals ; Biomarkers ; Biopterins/analogs & derivatives ; Biopterins/pharmacology ; Catalysis ; Cellular Senescence/drug effects ; Disease Models, Animal ; Disease Susceptibility ; Heart Diseases/etiology ; Heart Diseases/metabolism ; Heart Diseases/pathology ; Heart Diseases/physiopathology ; Humans ; Liver/drug effects ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Models, Biological ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Phenylalanine/blood ; Phenylalanine/metabolism ; Rats
    Chemische Substanzen Amino Acids ; Biomarkers ; Biopterins ; Phenylalanine (47E5O17Y3R) ; sapropterin (EGX657432I)
    Sprache Englisch
    Erscheinungsdatum 2021-06-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.121.054204
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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